Volume 12, Issue 14

Alpha-ketoglutarate for adipose tissue rejuvenation

Qiyu Tian, Xiangdong Liu, Min Du,

https://doi.org/10.18632/aging.103853 pp 13845—13846

PDF How to Cite Request Reprint

Cite this Article

How to cite

Tian Q, Liu X, Du M, . Alpha-ketoglutarate for adipose tissue rejuvenation. . 12:13845-13846. https://doi.org/10.18632/aging.103853

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

Cerebrovascular dysfunction links aging to neurological disease

Candice E. Van Skike, Veronica Galvan,

https://doi.org/10.18632/aging.103854 pp 13847—13848

PDF How to Cite Request Reprint

COVID-19
High neutrophil-to-lymphocyte ratio associated with progression to critical illness in older patients with COVID-19: a multicenter retrospective study

Jiangshan Lian, Ciliang jin, Shaorui Hao, Xiaoli Zhang, Meifang Yang, Xi Jin, Yingfeng Lu, Jianhua Hu, Shanyan Zhang, Lin Zheng, Hongyu Jia, Huan Cai, Yimin Zhang, Guodong Yu, Xiaoyan Wang, Jueqing Gu, Chanyuan Ye, Xiaopeng Yu, Jianguo Gao, Yida Yang, Jifang Sheng,

https://doi.org/10.18632/aging.103582 pp 13849—13859

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lian J, jin C, Hao S, Zhang X, Yang M, Jin X, Lu Y, Hu J, Zhang S, Zheng L, Jia H, Cai H, Zhang Y, et al, . High neutrophil-to-lymphocyte ratio associated with progression to critical illness in older patients with COVID-19: a multicenter retrospective study. . 12:13849-13859. https://doi.org/10.18632/aging.103582

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lian, Jiangshan 
                AU  - jin, Ciliang 
                AU  - Hao, Shaorui 
                AU  - Zhang, Xiaoli 
                AU  - Yang, Meifang 
                AU  - Jin, Xi 
                AU  - Lu, Yingfeng 
                AU  - Hu, Jianhua 
                AU  - Zhang, Shanyan 
                AU  - Zheng, Lin 
                AU  - Jia, Hongyu 
                AU  - Cai, Huan 
                AU  - Zhang, Yimin 
                AU  - Yu, Guodong 
                AU  - Wang, Xiaoyan 
                AU  - Gu, Jueqing 
                AU  - Ye, Chanyuan 
                AU  - Yu, Xiaopeng 
                AU  - Gao, Jianguo 
                AU  - Yang, Yida 
                AU  - Sheng, Jifang 
                TI  - High neutrophil-to-lymphocyte ratio associated with progression to critical illness in older patients with COVID-19: a multicenter retrospective study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103582
                DO  - 10.18632/aging.103582
                SP  - 13849
                EP  - 13859
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lian, Jiangshan 
                AU  - jin, Ciliang 
                AU  - Hao, Shaorui 
                AU  - Zhang, Xiaoli 
                AU  - Yang, Meifang 
                AU  - Jin, Xi 
                AU  - Lu, Yingfeng 
                AU  - Hu, Jianhua 
                AU  - Zhang, Shanyan 
                AU  - Zheng, Lin 
                AU  - Jia, Hongyu 
                AU  - Cai, Huan 
                AU  - Zhang, Yimin 
                AU  - Yu, Guodong 
                AU  - Wang, Xiaoyan 
                AU  - Gu, Jueqing 
                AU  - Ye, Chanyuan 
                AU  - Yu, Xiaopeng 
                AU  - Gao, Jianguo 
                AU  - Yang, Yida 
                AU  - Sheng, Jifang 
                TI  - High neutrophil-to-lymphocyte ratio associated with progression to critical illness in older patients with COVID-19: a multicenter retrospective study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103582
                DO  - 10.18632/aging.103582
                SP  - 13849
                EP  - 13859
                PY  - 
                AB  - This retrospective cohort study aimed to investigate the correlation of the neutrophil-to-lymphocyte ratio (NLR) with critical illness in older patients with COVID-19, and evaluate the prognostic power of the NLR at admission. We enrolled 232 patients with COVID-19, aged &#x2265;60 y, in Zhejiang province from January 17 to March 3, 2020. Primary outcomes were evaluated until April 13. Cox regression was performed for prognostic factors. Twenty-nine (12.5%) patients progressed to critical illness. Age, shortness of breath, comorbidities including hypertension, heart disease, and chronic obstructive pulmonary disease, higher NLR, lower albumin levels, and multiple mottling and ground-glass opacity were associated with progression. In the multivariate analysis, older age (hazard ratio [HR] 1.121, confidence interval [CI] 1.070-1.174, P&lt;0.001), heart disease (HR 2.587, CI 1.156-5.787, P=0.021), higher NLR (HR 1.136, CI 1.094-1.180, P &lt; 0.001), and multiple mottling and ground-glass opacity (HR 4.518, CI 1.906-10.712, P&lt;0.001) remained critical illness predictors. The NLR was independently associated with progression to critical illness; the relationship was significant and graded (HR: 1.16 per unit; 95% CI: 1.10-1.22; P for trend &lt; 0.001). Therefore, NLR can be adopted as a prognostic tool to assist healthcare providers predict the clinical outcomes of older patients suffering from COVID-19.
                ER  -

Click to copy this citation from the text box above or download the citation:

COVID-19
Clinical imaging characteristics of inpatients with coronavirus disease-2019 in Heilongjiang Province, China: a retrospective study

Hao Jiang, Wei Guo, Zhongxing Shi, Huijie Jiang, Mingyu Zhang, Lai Wei, Yongmei Pan,

https://doi.org/10.18632/aging.103633 pp 13860—13868

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Jiang H, Guo W, Shi Z, Jiang H, Zhang M, Wei L, Pan Y, . Clinical imaging characteristics of inpatients with coronavirus disease-2019 in Heilongjiang Province, China: a retrospective study. . 12:13860-13868. https://doi.org/10.18632/aging.103633

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Jiang, Hao 
                AU  - Guo, Wei 
                AU  - Shi, Zhongxing 
                AU  - Jiang, Huijie 
                AU  - Zhang, Mingyu 
                AU  - Wei, Lai 
                AU  - Pan, Yongmei 
                TI  - Clinical imaging characteristics of inpatients with coronavirus disease-2019 in Heilongjiang Province, China: a retrospective study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103633
                DO  - 10.18632/aging.103633
                SP  - 13860
                EP  - 13868
                PY  - 
                AB  - Objective: To investigate the clinical, laboratory, and radiological characteristics of patients with coronavirus disease-2019 (COVID-19) in Heilongjiang Province.Results: Patients in the ICU group were older and their incidence of cardiovascular disease was higher than those in the non-ICU group. Lymphocyte levels were lower and neutrophil and D-dimer levels were higher in the ICU than that in the non-ICU group. Compared to the non-ICU group, the incidence of pulmonary consolidation and ground-glass opacity with consolidation was significantly higher in the ICU group, all lung lobes were more likely to be involved, with higher number of lung lobes and areas surrounding the bronchi. Of the 59 patients with COVID-19 in this group, 15 received mechanical ventilation. All intubated patients involved lung lobes, and a large number of lesions were observed in the area around the bronchial vessels.Conclusion: Significant differences were observed in clinical symptoms, laboratory tests, and computed tomography features between the ICU and non-ICU groups.Methods: A total of 59 patients with COVID-19, comprising 44 patients in the intensive care unit (ICU) and 15 in the non-ICU, were retrospectively analyzed. Characteristics of the two groups of patients were compared.
                ER  -

Click to copy this citation from the text box above or download the citation:

COVID-19
Risk of death by age and gender from CoVID-19 in Peru, March-May, 2020

Cesar Munayco, Gerardo Chowell, Amna Tariq, Eduardo A. Undurraga, Kenji Mizumoto,

https://doi.org/10.18632/aging.103687 pp 13869—13881

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Munayco C, Chowell G, Tariq A, Undurraga EA, Mizumoto K, . Risk of death by age and gender from CoVID-19 in Peru, March-May, 2020. . 12:13869-13881. https://doi.org/10.18632/aging.103687

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Munayco, Cesar 
                AU  - Chowell, Gerardo 
                AU  - Tariq, Amna 
                AU  - Undurraga, Eduardo A. 
                AU  - Mizumoto, Kenji 
                TI  - Risk of death by age and gender from CoVID-19 in Peru, March-May, 2020
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103687
                DO  - 10.18632/aging.103687
                SP  - 13869
                EP  - 13881
                PY  - 
                AB  - Peru implemented strict social distancing measures during the early phase of the epidemic and is now experiencing one of the largest CoVID-19 epidemics in Latin America. Estimates of disease severity are an essential indicator to inform policy decisions about the intensity and duration of interventions needed to mitigate the outbreak. Here we derive delay-adjusted case fatality risks (aCFR) of CoVID-19 in a middle-income country in South America.We utilize government-reported time series of CoVID-19 cases and deaths in Peru stratified by age group and gender.As of May 25, 2020, we estimate the aCFR for men and women at 10.8% (95%CrI: 10.5-11.1%) and 6.5% (95%CrI: 6.2-6.8%), respectively, whereas the overall aCFR was estimated at 9.1% (95%CrI: 8.9-9.3%). Our results show that senior individuals have been the most severely affected by CoVID-19, particularly men, with an aCFR of nearly 60% for those aged 80- years. We also found that men have a significantly higher cumulative morbidity ratio across most age groups (proportion test, p-value&lt; 0.001), with the exception of those aged 0-9 years.The ongoing CoVID-19 pandemic is generating a substantial mortality burden in Peru. Senior individuals, especially those older than 70 years, are being disproportionately affected by the CoVID-19 pandemic.
                ER  -

Click to copy this citation from the text box above or download the citation:

COVID-19
Development and validation of a risk stratification model for screening suspected cases of COVID-19 in China

Jing Ma, Xiaowei Shi, Weiming Xu, Feifei Lv, Jian Wu, Qiaoling Pan, Jinfeng Yang, Jiong Yu, Hongcui Cao, Lanjuan Li,

https://doi.org/10.18632/aging.103694 pp 13882—13894

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ma J, Shi X, Xu W, Lv F, Wu J, Pan Q, Yang J, Yu J, Cao H, Li L, . Development and validation of a risk stratification model for screening suspected cases of COVID-19 in China. . 12:13882-13894. https://doi.org/10.18632/aging.103694

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ma, Jing 
                AU  - Shi, Xiaowei 
                AU  - Xu, Weiming 
                AU  - Lv, Feifei 
                AU  - Wu, Jian 
                AU  - Pan, Qiaoling 
                AU  - Yang, Jinfeng 
                AU  - Yu, Jiong 
                AU  - Cao, Hongcui 
                AU  - Li, Lanjuan 
                TI  - Development and validation of a risk stratification model for screening suspected cases of COVID-19 in China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103694
                DO  - 10.18632/aging.103694
                SP  - 13882
                EP  - 13894
                PY  - 
                AB  - How to quickly identify high-risk populations is critical to epidemic control. We developed and validated a risk prediction model for screening SARS-CoV-2 infection in suspected cases with an epidemiological history. A total of 1019 patients, &#x2265;13 years of age, who had an epidemiological history were enrolled from fever clinics between January 2020 and February 2020. Among 103 (10.11%) cases of COVID-19 were confirmed. Multivariable analysis summarized four features associated with increased risk of SARS-CoV-2 infection, summarized in the mnemonic COVID-19-REAL: radiological evidence of pneumonia (1 point), eosinophils &lt; 0.005 &#xD7; 109/L (1 point), age &#x2265; 32 years (2 points), and leukocytes &lt; 6.05 &#xD7; 109 /L (1 point). The area under the ROC curve for the training group was 0.863 (95% CI, 0.813 - 0.912). A cut-off value of less than 3 points for COVID-19-REAL was assigned to define the low-risk population. Only 10 (2.70%) of 371 patients were proved to be SARS-CoV-2 positive, with a negative predictive value of 0.973. External validation was similar. This study provides a simple, practical, and robust screening model, COVID-19-REAL, able to identify populations at high risk for SARS-CoV-2 infection.
                ER  -

Click to copy this citation from the text box above or download the citation:

COVID-19
COVID-19 induced liver function abnormality associates with age

Shasha Li, Jinsong Li, Zhenhua Zhang, Lin Tan, Tuo Shao, Ming Li, Xiuyong Li, Jacinta A. Holmes, Wenyu Lin, Mingfeng Han,

https://doi.org/10.18632/aging.103720 pp 13895—13904

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li S, Li J, Zhang Z, Tan L, Shao T, Li M, Li X, Holmes JA, Lin W, Han M, . COVID-19 induced liver function abnormality associates with age. . 12:13895-13904. https://doi.org/10.18632/aging.103720

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Shasha 
                AU  - Li, Jinsong 
                AU  - Zhang, Zhenhua 
                AU  - Tan, Lin 
                AU  - Shao, Tuo 
                AU  - Li, Ming 
                AU  - Li, Xiuyong 
                AU  - Holmes, Jacinta A. 
                AU  - Lin, Wenyu 
                AU  - Han, Mingfeng 
                TI  - COVID-19 induced liver function abnormality associates with age
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103720
                DO  - 10.18632/aging.103720
                SP  - 13895
                EP  - 13904
                PY  - 
                AB  - Background: Coronavirus disease 2019 (COVID-19) is a novel infectious disease that may cause fever, dry cough, fatigue and shortness of breath. The impact of COVID-19 on liver function is not well described.Results: We found that the overall frequency of LFT abnormality was 17.6%. Frequency of LFT abnormality was significantly greater in patients with severe/critical (SC) COVID-19 compared to those with mild/moderate (MM) COVID-19 (32.4% vs 11.6%, p=0.011). Among patients with LFT abnormality, the median age was significantly higher in the SC group compared to the MM group (52 vs 39 years, p=0.021).Conclusion: COVID-19 is frequently associated with mild liver function abnormality, particularly in individuals with severe/critical COVID-19 who were older. Liver function should be monitored carefully during infection, with judicious use of hepatotoxic agents where possible and avoidance of prolonged hypotension to minimize liver injury in older patients.Methods: The No. 2 People&#x2019;s Hospital of Fuyang City in China has admitted a total of 159 patients with confirmed COVID-19 since the outbreak from January 2020 to March 2020. We analyzed the incidence of liver function test (LFT) abnormality in these patients with confirmed COVID-19 infection.
                ER  -

Click to copy this citation from the text box above or download the citation:

Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration

Sara Romero-Vázquez, Alfredo Adán, Marc Figueras-Roca, Victor Llorenç, Mark Slevin, Gemma Vilahur, Lina Badimon, Andrew D Dick, Blanca Molins,

https://doi.org/10.18632/aging.103655 pp 13905—13923

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Romero-Vázquez S, Adán A, Figueras-Roca M, Llorenç V, Slevin M, Vilahur G, Badimon L, Dick AD, Molins B, . Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration. . 12:13905-13923. https://doi.org/10.18632/aging.103655

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Romero-Vázquez, Sara 
 AU - Adán, Alfredo 
 AU - Figueras-Roca, Marc 
 AU - Llorenç, Victor 
 AU - Slevin, Mark 
 AU - Vilahur, Gemma 
 AU - Badimon, Lina 
 AU - Dick, Andrew D 
 AU - Molins, Blanca 
 TI - Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103655
 DO - 10.18632/aging.103655
 SP - 13905
 EP - 13923
 PY - 
 AB - The retinal pigment epithelium (RPE) is considered one of the main targets of age-related macular degeneration (AMD), the leading cause of irreversible vision loss among the ageing population worldwide. Persistent low grade inflammation and oxidative stress eventually lead to RPE dysfunction and disruption of the outer blood-retinal barrier (oBRB). Increased levels of circulating pentameric C-reactive protein (pCRP) are associated with higher risk of AMD. The monomeric form (mCRP) has been detected in drusen, the hallmark deposits associated with AMD, and we have found that mCRP induces oBRB disruption. However, it is unknown how mCRP is generated in the subretinal space. Using a Transwell model we found that both pCRP and mCRP can cross choroidal endothelial cells and reach the RPE in vitro and that mCRP, but not pCRP, is able to cross the RPE monolayer in ARPE-19 cells. Alternatively, mCRP can originate from the dissociation of pCRP in the surface of lipopolysaccharide-damaged RPE in both ARPE-19 and primary porcine RPE lines. In addition, we found that the proinflammatory phenotype of mCRP in the RPE depends on its topological localization. Together, our findings further support mCRP contribution to AMD progression enhancing oBRB disruption.
 ER -

Click to copy this citation from the text box above or download the citation:

_{Remifentanil preconditioning protects against hypoxia-induced senescence and necroptosis in human cardiac myocytes in vitro}

Anna Lewinska, Jagoda Adamczyk-Grochala, Dominika Bloniarz, Beata Horeczy, Slawomir Zurek, Arkadiusz Kurowicki, Bogumila Woloszczuk-Gebicka, Kazimierz Widenka, Maciej Wnuk,

https://doi.org/10.18632/aging.103604 pp 13924—13938

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lewinska A, Adamczyk-Grochala J, Bloniarz D, Horeczy B, Zurek S, Kurowicki A, Woloszczuk-Gebicka B, Widenka K, Wnuk M, . _{Remifentanil preconditioning protects against hypoxia-induced senescence and necroptosis in human cardiac myocytes in vitro}. . 12:13924-13938. https://doi.org/10.18632/aging.103604

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Lewinska, Anna 
 AU - Adamczyk-Grochala, Jagoda 
 AU - Bloniarz, Dominika 
 AU - Horeczy, Beata 
 AU - Zurek, Slawomir 
 AU - Kurowicki, Arkadiusz 
 AU - Woloszczuk-Gebicka, Bogumila 
 AU - Widenka, Kazimierz 
 AU - Wnuk, Maciej 
 TI - Remifentanil preconditioning protects against hypoxia-induced senescence and necroptosis in human cardiac myocytes in vitro
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103604
 DO - 10.18632/aging.103604
 SP - 13924
 EP - 13938
 PY - 
 AB - Remifentanil and other opioids are suggested to be protective against ischemia-reperfusion injury in animal models and coronary artery bypass surgery patients, however the molecular basis of such protection is far from being understood. In the present study, we have used a model of human cardiomyocytes treated with the hypoxia-mimetic agent cobalt chloride to investigate remifentanil preconditioning-based adaptive responses and underlying mechanisms. Hypoxic conditions promoted oxidative and nitrosative stress, p21-mediated cellular senescence and the activation of necroptotic pathway that was accompanied by a 2.2-, 9.6- and 8.2-fold increase in phosphorylation status of mixed lineage kinase domain-like pseudokinase (MLKL) and release of pro-inflammatory cytokine IL-8 and cardiac troponin I, a marker of myocardial damage, respectively. Remifentanil preconditioning was able to lower hypoxia-mediated protein carbonylation and limit MLKL-based signaling and pro-inflammatory response to almost normoxic control levels, and decrease hypoxia-induced pro-senescent activity of about 21% compared to control hypoxic conditions. In summary, we have shown for the first time that remifentanil can protect human cardiomyocytes against hypoxia-induced cellular senescence and necroptosis that may have importance with respect to the use of remifentanil to diminish myocardial ischemia and reperfusion injury in patients undergoing cardiac surgery.
 ER -

Click to copy this citation from the text box above or download the citation:

Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice

Emanuela Agosti, Marilisa De Feudis, Elia Angelino, Roberta Belli, Maraiza Alves Teixeira, Ivan Zaggia, Edoardo Tamiso, Tommaso Raiteri, Andrea Scircoli, Flavio L. Ronzoni, Maurizio Muscaritoli, Andrea Graziani, Flavia Prodam, Maurilio Sampaolesi, Paola Costelli, Elisabetta Ferraro, Simone Reano, Nicoletta Filigheddu,

https://doi.org/10.18632/aging.103802 pp 13939—13957

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Agosti E, De Feudis M, Angelino E, Belli R, Alves Teixeira M, Zaggia I, Tamiso E, Raiteri T, Scircoli A, Ronzoni FL, Muscaritoli M, Graziani A, Prodam F, et al, . Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice. . 12:13939-13957. https://doi.org/10.18632/aging.103802

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Agosti, Emanuela 
                AU  - De Feudis, Marilisa 
                AU  - Angelino, Elia 
                AU  - Belli, Roberta 
                AU  - Alves Teixeira, Maraiza 
                AU  - Zaggia, Ivan 
                AU  - Tamiso, Edoardo 
                AU  - Raiteri, Tommaso 
                AU  - Scircoli, Andrea 
                AU  - Ronzoni, Flavio L. 
                AU  - Muscaritoli, Maurizio 
                AU  - Graziani, Andrea 
                AU  - Prodam, Flavia 
                AU  - Sampaolesi, Maurilio 
                AU  - Costelli, Paola 
                AU  - Ferraro, Elisabetta 
                AU  - Reano, Simone 
                AU  - Filigheddu, Nicoletta 
                TI  - Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103802
                DO  - 10.18632/aging.103802
                SP  - 13939
                EP  - 13957
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Agosti, Emanuela 
                AU  - De Feudis, Marilisa 
                AU  - Angelino, Elia 
                AU  - Belli, Roberta 
                AU  - Alves Teixeira, Maraiza 
                AU  - Zaggia, Ivan 
                AU  - Tamiso, Edoardo 
                AU  - Raiteri, Tommaso 
                AU  - Scircoli, Andrea 
                AU  - Ronzoni, Flavio L. 
                AU  - Muscaritoli, Maurizio 
                AU  - Graziani, Andrea 
                AU  - Prodam, Flavia 
                AU  - Sampaolesi, Maurilio 
                AU  - Costelli, Paola 
                AU  - Ferraro, Elisabetta 
                AU  - Reano, Simone 
                AU  - Filigheddu, Nicoletta 
                TI  - Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103802
                DO  - 10.18632/aging.103802
                SP  - 13939
                EP  - 13957
                PY  - 
                AB  - Sarcopenia, the decline in muscle mass and functionality during aging, might arise from age-associated endocrine dysfunction. Ghrelin is a hormone circulating in both acylated (AG) and unacylated (UnAG) forms with anti-atrophic activity on skeletal muscle. Here, we show that not only lifelong overexpression of UnAG (Tg) in mice, but also the deletion of ghrelin gene (Ghrl KO) attenuated the age-associated muscle atrophy and functionality decline, as well as systemic inflammation. Yet, the aging of Tg and Ghrl KO mice occurs with different dynamics: while old Tg mice seem to preserve the characteristics of young animals, Ghrl KO mice features deteriorate with aging. However, young Ghrl KO mice show more favorable traits compared to WT animals that result, on the whole, in better performances in aged Ghrl KO animals. Treatment with pharmacological doses of UnAG improved muscle performance in old mice without modifying the feeding behavior, body weight, and adipose tissue mass. The antiatrophic effect on muscle mass did not correlate with modifications of protein catabolism. However, UnAG treatment induced a strong shift towards oxidative metabolism in muscle. Altogether, these data confirmed and expanded some of the previously reported findings and advocate for the design of UnAG analogs to treat sarcopenia.
                ER  -

Click to copy this citation from the text box above or download the citation:

Decreased autophagy and fuel switching occur in a senescent hepatic cell model system

Brijesh Kumar Singh, Madhulika Tripathi, Reddemma Sandireddy, Keziah Tikno, Jin Zhou, Paul Michael Yen,

https://doi.org/10.18632/aging.103740 pp 13958—13978

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Singh BK, Tripathi M, Sandireddy R, Tikno K, Zhou J, Yen PM, . Decreased autophagy and fuel switching occur in a senescent hepatic cell model system. . 12:13958-13978. https://doi.org/10.18632/aging.103740

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Singh, Brijesh Kumar 
                AU  - Tripathi, Madhulika 
                AU  - Sandireddy, Reddemma 
                AU  - Tikno, Keziah 
                AU  - Zhou, Jin 
                AU  - Yen, Paul Michael 
                TI  - Decreased autophagy and fuel switching occur in a senescent hepatic cell model system
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103740
                DO  - 10.18632/aging.103740
                SP  - 13958
                EP  - 13978
                PY  - 
                AB  - Although aging in the liver contributes to the development of chronic liver diseases such as NAFLD and insulin resistance, little is known about the molecular and metabolic details of aging in hepatic cells. To examine these issues, we used sequential oxidative stress with hydrogen peroxide to induce premature senescence in AML12 hepatic cells. The senescent cells exhibited molecular and metabolic signatures, increased SA-&#x3B2;Gal and &#x3B3;H2A.X staining, and elevated senescence and pro-inflammatory gene expression that resembled livers from aged mice. Metabolic phenotyping showed fuel switching towards glycolysis and mitochondrial glutamine oxidation as well as impaired energy production. The senescent AML12 cells also had increased mTOR signaling and decreased autophagy which likely contributed to the fuel switching from &#x3B2;-oxidation that occurred in normal AML12 cells. Additionally, senescence-associated secretory phenotype (SASP) proteins from conditioned media of senescent cells sensitized normal AML12 cells to palmitate-induced toxicity, a known pathological effect of hepatic aging. In summary, we have generated senescent AML12 cells which displayed the molecular hallmarks of aging and also exhibited the aberrant metabolic phenotype, mitochondrial function, and cell signaling that occur in the aged liver.
                ER  -

Click to copy this citation from the text box above or download the citation:

Senescence-like phenotype in post-mitotic cells of mice entering middle age

Marco Raffaele, Kristina Kovacovicova, Francesca Bonomini, Rita Rezzani, Jan Frohlich, Manlio Vinciguerra,

https://doi.org/10.18632/aging.103637 pp 13979—13990

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Raffaele M, Kovacovicova K, Bonomini F, Rezzani R, Frohlich J, Vinciguerra M, . Senescence-like phenotype in post-mitotic cells of mice entering middle age. . 12:13979-13990. https://doi.org/10.18632/aging.103637

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Raffaele, Marco 
                AU  - Kovacovicova, Kristina 
                AU  - Bonomini, Francesca 
                AU  - Rezzani, Rita 
                AU  - Frohlich, Jan 
                AU  - Vinciguerra, Manlio 
                TI  - Senescence-like phenotype in post-mitotic cells of mice entering middle age
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103637
                DO  - 10.18632/aging.103637
                SP  - 13979
                EP  - 13990
                PY  - 
                AB  - Staining mice tissues for &#x3B2;-galactosidase activity is a fundamental tool to detect age- or disease-associated cellular senescence. However, reported analyses of positivity for senescence-associated &#x3B2;-galactosidase activity or for other markers of senescence in post-mitotic cells of healthy murine tissues have been fragmentary or inconclusive. Here, we attempted to independently deepen this knowledge using multiple senescence markers within the same cells of wild type mice entering middle age (9 months of age). A histochemistry protocol for the pH-dependent detection of &#x3B2;-galactosidase activity in several tissues was used. At pH 6, routinely utilized to detect senescence-associated &#x3B2;-galactosidase activity, only specific cellular populations in the mouse body (including Purkinje cells and choroid plexus in the central nervous system) were detected as strongly positive for &#x3B2;-galactosidase activity. These post-mitotic cells were also positive for other established markers of senescence (p16, p21 and DPP4), detected by immunofluorescence, confirming a potential senescent phenotype. These data might contribute to understanding the functional relation between the senescence-associated &#x3B2;-galactosidase activity and senescence markers in post-mitotic cells in absence of disease or advanced aging.
                ER  -

Click to copy this citation from the text box above or download the citation:

Peanut skin extract ameliorates the symptoms of type 2 diabetes mellitus in mice by alleviating inflammation and maintaining gut microbiota homeostasis

Lan Xiang, Qiaobei Wu, Hiroyuki Osada, Minoru Yoshida, Wensheng Pan, Jianhua Qi,

https://doi.org/10.18632/aging.103521 pp 13991—14018

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xiang L, Wu Q, Osada H, Yoshida M, Pan W, Qi J, . Peanut skin extract ameliorates the symptoms of type 2 diabetes mellitus in mice by alleviating inflammation and maintaining gut microbiota homeostasis. . 12:13991-14018. https://doi.org/10.18632/aging.103521

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xiang, Lan 
                AU  - Wu, Qiaobei 
                AU  - Osada, Hiroyuki 
                AU  - Yoshida, Minoru 
                AU  - Pan, Wensheng 
                AU  - Qi, Jianhua 
                TI  - Peanut skin extract ameliorates the symptoms of type 2 diabetes mellitus in mice by alleviating inflammation and maintaining gut microbiota homeostasis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103521
                DO  - 10.18632/aging.103521
                SP  - 13991
                EP  - 14018
                PY  - 
                AB  - In this study, mice with type 2 diabetes mellitus (T2DM) induced by high-fat diet were used to investigate the antidiabetic effect and mechanism of action of peanut skin extract (PSE). Results revealed that the fasting blood glucose, body weight, and food intake of mice with T2DM significantly decreased after they were given PSE. The effects of 80 mg/kg PSE were similar to those of 140 mg/kg metformin (MET). The glucose tolerance and insulin sensitivity of the mice also improved. The composition of intestinal microflora in the mice significantly changed after PSE administration. In particular, no Actinobacteria was detected in the PSE-treated group, and the ratio of Firmicutes to Bacteroidetes was remarkably reduced. PSE also increased the abundance of gut microbiota involved in fatty acid biosynthesis, lipid biosynthesis, and sucrose metabolism. The abundance of gut microbiota related to aminoacyl-tRNA biosynthesis also decreased. Lipopolysaccharide, interleukin (IL)-6, IL-1&#x3B2; and tumor necrosis factor-&#x3B1; in the blood, liver and adipose tissue were reduced by PSE. Similarly, the mRNA expression levels of IkappaB kinase and nuclear factor kappaB in the hypothalamus were reduced by PSE. These results suggested that PSE and MET elicited significant antidiabetic effects by maintaining gut microbiota and inhibiting inflammation.
                ER  -

Click to copy this citation from the text box above or download the citation:

Metformin administration during pregnancy attenuated the long-term maternal metabolic and cognitive impairments in a mouse model of gestational diabetes

Yalan Zhao, Xiaobo Zhou, Xue Zhao, Xinyang Yu, Andi Wang, Xuyang Chen, Hongbo Qi, Ting-Li Han, Hua Zhang, Philip N. Baker,

https://doi.org/10.18632/aging.103505 pp 14019—14036

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhao Y, Zhou X, Zhao X, Yu X, Wang A, Chen X, Qi H, Han T, Zhang H, Baker PN, . Metformin administration during pregnancy attenuated the long-term maternal metabolic and cognitive impairments in a mouse model of gestational diabetes. . 12:14019-14036. https://doi.org/10.18632/aging.103505

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhao, Yalan 
                AU  - Zhou, Xiaobo 
                AU  - Zhao, Xue 
                AU  - Yu, Xinyang 
                AU  - Wang, Andi 
                AU  - Chen, Xuyang 
                AU  - Qi, Hongbo 
                AU  - Han, Ting-Li 
                AU  - Zhang, Hua 
                AU  - Baker, Philip N. 
                TI  - Metformin administration during pregnancy attenuated the long-term maternal metabolic and cognitive impairments in a mouse model of gestational diabetes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103505
                DO  - 10.18632/aging.103505
                SP  - 14019
                EP  - 14036
                PY  - 
                AB  - Background: Gestational diabetes mellitus (GDM) is a metabolic disease that can have long-term adverse effects on the cognitive function of mothers. In our study, we explored the changes in metabolic health and cognitive function in mice of middle- and old- age after exposure to GDM, and whether metformin therapy during pregnancy provided long-term benefits.Results: Mice with GDM demonstrated significant cognitive impairment in old age, which was associated with insulin resistance. Gestational metformin therapy was shown to increase insulin sensitivity and improve cognition. The ovarian aging rate was also accelerated in mice exposed to GDM during pregnancy, which may be related to fatty acid metabolism in the ovaries.Conclusion: Treatment with metformin during pregnancy was shown to improve fatty acid metabolism in ovarian tissues.Method: During pregnancy, mice were fed with a high-fat diet (GDM group) or a low-fat diet (Control group), and a third group received metformin while receiving a high-fat diet (Treatment group). At 12 months old, the mice completed an oral glucose tolerance test, insulin tolerance test, Morris water maze test, female sex hormones were measured, and metabolite profiles of tissue from the ovaries, hypothalamus, and pituitary glands were analysed using gas chromatography-mass spectrometry.
                ER  -

Click to copy this citation from the text box above or download the citation:

Calponin 3 is associated with poor prognosis and regulates proliferation and metastasis in osteosarcoma

Fei Dai, Fei Luo, Rui Zhou, Qiang Zhou, Jianzhong Xu, Zehua Zhang, Jun Xiao, Lei Song,

https://doi.org/10.18632/aging.103224 pp 14037—14049

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Dai F, Luo F, Zhou R, Zhou Q, Xu J, Zhang Z, Xiao J, Song L, . Calponin 3 is associated with poor prognosis and regulates proliferation and metastasis in osteosarcoma. . 12:14037-14049. https://doi.org/10.18632/aging.103224

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Dai, Fei 
                AU  - Luo, Fei 
                AU  - Zhou, Rui 
                AU  - Zhou, Qiang 
                AU  - Xu, Jianzhong 
                AU  - Zhang, Zehua 
                AU  - Xiao, Jun 
                AU  - Song, Lei 
                TI  - Calponin 3 is associated with poor prognosis and regulates proliferation and metastasis in osteosarcoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103224
                DO  - 10.18632/aging.103224
                SP  - 14037
                EP  - 14049
                PY  - 
                AB  - Osteosarcoma is a malignant, life-threatening tumor that affects children and adolescents. In this study, we identified high levels of calponin 3 (CNN3) protein in osteosarcoma tissues and cell lines. The receiver operating characteristic curve analysis revealed that CNN3 has diagnostic value for patients with osteosarcoma. We also found that high CNN3 expression was associated with tumor size, tumor stage, and lymph node and distant metastases. Moreover, high levels of CNN3 mRNA were associated with a poor overall survival rate and a shorter disease-free survival period. CNN3 silencing inhibited cell proliferation, induced apoptosis and cell cycle arrest at the G1 stage, and inhibited cell migration and invasion in vitro. Furthermore, CNN3 silencing also inhibited subcutaneous tumor growth and lung metastasis in vivo. Western blotting revealed that silencing of CNN3 resulted in downregulated expression of MMP9, VEGF, and vimentin, and upregulation of E-cadherin. CNN3 silencing also resulted in downregulation of the ERK1/2 and p38 signaling pathways. In conclusion, high CNN3 expression was found to help in the diagnosis of osteosarcoma, and was found to be associated with poor prognosis in patients. Therefore, CNN3 may play an oncogenic role during the progression of osteosarcoma by activating the ERK1/2 and p38 pathways.
                ER  -

Click to copy this citation from the text box above or download the citation:

Dehydroandrographolide inhibits mastitis by activating autophagy without affecting intestinal flora

Wenjin Guo, Juxiong Liu, Yufei Zhang, He Ma, Yuhang Li, Qian Gong, Yu Cao, Guiqiu Hu, Shengnan Xie, Shoupeng Fu,

https://doi.org/10.18632/aging.103312 pp 14050—14065

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Guo W, Liu J, Zhang Y, Ma H, Li Y, Gong Q, Cao Y, Hu G, Xie S, Fu S, . Dehydroandrographolide inhibits mastitis by activating autophagy without affecting intestinal flora. . 12:14050-14065. https://doi.org/10.18632/aging.103312

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Guo, Wenjin 
                AU  - Liu, Juxiong 
                AU  - Zhang, Yufei 
                AU  - Ma, He 
                AU  - Li, Yuhang 
                AU  - Gong, Qian 
                AU  - Cao, Yu 
                AU  - Hu, Guiqiu 
                AU  - Xie, Shengnan 
                AU  - Fu, Shoupeng 
                TI  - Dehydroandrographolide inhibits mastitis by activating autophagy without affecting intestinal flora
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103312
                DO  - 10.18632/aging.103312
                SP  - 14050
                EP  - 14065
                PY  - 
                AB  - Mastitis can seriously damage the physical and mental health of lactating women. The use of antibiotics and anti-inflammatory drugs may damage the flora balance in lactating women. To alleviate mastitis in lactating women and reduce drug-induced damage to the flora, we found that dehydroandrographolide (Deh) has good anti-inflammatory and bacterial balance functions. In vivo, we found that Deh significantly inhibited the expression of MPO, IL6, IL-1&#x3B2;, TNF-&#x3B1;, COX2 and iNOS and reduced pathological damage to the mammary gland. The feces in the control and Deh groups were collected and sequenced for 16S flora. The results showed that Deh did not change the primary intestinal microflora composition of the two groups. In vitro, our study showed that Deh significantly inhibited the expression of IL6, IL-1&#x3B2; and TNF-&#x3B1; in the EpH4-Ev cell line. When an AMPK inhibitor was added, the anti-inflammatory effect of Deh was blocked. To further study the anti-inflammatory mechanism of Deh, we found that Deh significantly promoted autophagy through the phosphorylation of AMPK, Beclin and ULK1. In conclusion, our study found that Deh promoted autophagy and played an anti-inflammatory role by activating the AMPK/Beclin/ULK1 signaling pathway and did not affect intestinal flora.
                ER  -

Click to copy this citation from the text box above or download the citation:

The achievement of comprehensive control targets among type 2 diabetes mellitus patients of different ages

Yun Yu, Kaipeng Xie, Qinglin Lou, Hui Xia, Dan Wu, Lingli Dai, Cuining Hu, Kunlin Wang, Shan Shan, Yun Hu, Wei Tang,

https://doi.org/10.18632/aging.103358 pp 14066—14079

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Yu Y, Xie K, Lou Q, Xia H, Wu D, Dai L, Hu C, Wang K, Shan S, Hu Y, Tang W, . The achievement of comprehensive control targets among type 2 diabetes mellitus patients of different ages. . 12:14066-14079. https://doi.org/10.18632/aging.103358

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Yu, Yun 
                AU  - Xie, Kaipeng 
                AU  - Lou, Qinglin 
                AU  - Xia, Hui 
                AU  - Wu, Dan 
                AU  - Dai, Lingli 
                AU  - Hu, Cuining 
                AU  - Wang, Kunlin 
                AU  - Shan, Shan 
                AU  - Hu, Yun 
                AU  - Tang, Wei 
                TI  - The achievement of comprehensive control targets among type 2 diabetes mellitus patients of different ages
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103358
                DO  - 10.18632/aging.103358
                SP  - 14066
                EP  - 14079
                PY  - 
                AB  - Objective: To evaluate achievement of comprehensive controls among patients with type 2 diabetes mellitus (T2DM) in different age groups.
                Results: The elderly patients had higher control rates for BMI (44.36%), TC (50.83%) and LDL-C (48.27%) than those aged 60-80 years and younger patients (all P &lt;0.05). Multiple logistic regression revealed that elderly patients were more likely to achieve control targets for HbA1c (odd ratio (OR) = 2.19), TC (OR = 1.32), HDL-C (OR = 1.35), and TG (OR = 1.74) than younger patients. This effect was stronger in males (ORHbA1c = 2.27; ORTC = 1.41; ORHDL-C = 1.51; ORTG = 1.80). By contrast, elderly females were only more likely to achieve HbA1c &lt; 7.0% (OR=1.88).
                Conclusions: Our findings suggest that comprehensive control strategies still should be strengthened.
                Methods: A total of 3126 T2DM patients were included, and detected blood pressure (BP), body mass index (BMI), glycosylated hemoglobin (HbA1c), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C). We divided patients into three age groups (&lt;60, 60-80 and &#x2265; 80 years), to assess the differences in achieving the control targets.
                ER  -

Click to copy this citation from the text box above or download the citation:

CircRNA FGFR3 induces epithelial-mesenchymal transition of ovarian cancer by regulating miR-29a-3p/E2F1 axis

Jing Zhou, Ze-Ning Dong, Bai-Quan Qiu, Ming Hu, Xiao-Qing Liang, Xing Dai, Dan Hong, Yu-Fang Sun,

https://doi.org/10.18632/aging.103388 pp 14080—14091

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhou J, Dong Z, Qiu B, Hu M, Liang X, Dai X, Hong D, Sun Y, . CircRNA FGFR3 induces epithelial-mesenchymal transition of ovarian cancer by regulating miR-29a-3p/E2F1 axis. . 12:14080-14091. https://doi.org/10.18632/aging.103388

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhou, Jing 
                AU  - Dong, Ze-Ning 
                AU  - Qiu, Bai-Quan 
                AU  - Hu, Ming 
                AU  - Liang, Xiao-Qing 
                AU  - Dai, Xing 
                AU  - Hong, Dan 
                AU  - Sun, Yu-Fang 
                TI  - CircRNA FGFR3 induces epithelial-mesenchymal transition of ovarian cancer by regulating miR-29a-3p/E2F1 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103388
                DO  - 10.18632/aging.103388
                SP  - 14080
                EP  - 14091
                PY  - 
                AB  - Circular RNAs (circRNAs) are a class of non-coding RNAs that regulate gene expression after transcription. However, the specific function of circRNAs in ovarian cancer remains undetermined. Previous studies have demonstrated abnormal expression of circFGFR3 in several cancers. The present study was designed to reveal the roles of circFGFR3 in ovarian cancer (OC). CircFGFR3 expression in OC tissues and cells was detected by RT-qPCR. The effects of CircFGFR3 on OC cells were evaluated by transwell assay and CCK-8 assay. Finally, the underlying mechanism was further revealed by luciferase reporter assay and western blotting. Our results showed that circFGFR3 expression was higher in OC cells and tissues than in normal ovarian cells and adjacent normal tissues; in addition, in OC patients, a high level of CircFGFR3 was related to lower survival rates and higher recurrence rates than a low level of circFGFR3. CircFGFR3 overexpression promotes OC progression by inducing epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, circFGFR3 upregulates E2F1 expression by sponging miR-29a-3p, and the overexpression of E2F1 or the suppression of miR-29a-3p induces OC cell EMT. Therefore, circFGFR3 serves as a promoter of OC by inducing OC cell EMT via the miR-29a-3p/E2F1 axis and circFGFR3 may be a prognostic biomarker for OC patients.
                ER  -

Click to copy this citation from the text box above or download the citation:

Blood DNA methylation sites predict death risk in a longitudinal study of 12, 300 individuals

Elena Colicino, Riccardo Marioni, Cavin Ward-Caviness, Rahul Gondalia, Weihua Guan, Brian Chen, Pei-Chien Tsai, Tianxiao Huan, Gao Xu, Agha Golareh, Joel Schwartz, Pantel Vokonas, Allan Just, John M. Starr, Allan F. McRae, Naomi R. Wray, Peter M. Visscher, Jan Bressler, Wen Zhang, Toshiko Tanaka, Ann Zenobia Moore, Luke C. Pilling, Guosheng Zhang, James D. Stewart, Yun Li, Lifang Hou, Juan Castillo-Fernandez, Tim Spector, Douglas P. Kiel, Joanne M. Murabito, Chunyu Liu, Mike Mendelson, Tim Assimes, Devin Absher, Phil S. Tsaho, Ake T. Lu, Luigi Ferrucci, Rory Wilson, Melanie Waldenberger, Holger Prokisch, Stefania Bandinelli, Jordana T. Bell, Daniel Levy, Ian J. Deary, Steve Horvath, Jim Pankow, Annette Peters, Eric A. Whitsel, Andrea Baccarelli,

https://doi.org/10.18632/aging.103408 pp 14092—14124

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Colicino E, Marioni R, Ward-Caviness C, Gondalia R, Guan W, Chen B, Tsai P, Huan T, Xu G, Golareh A, Schwartz J, Vokonas P, Just A, et al, . Blood DNA methylation sites predict death risk in a longitudinal study of 12, 300 individuals. . 12:14092-14124. https://doi.org/10.18632/aging.103408

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Colicino, Elena 
                AU  - Marioni, Riccardo 
                AU  - Ward-Caviness, Cavin 
                AU  - Gondalia, Rahul 
                AU  - Guan, Weihua 
                AU  - Chen, Brian 
                AU  - Tsai, Pei-Chien 
                AU  - Huan, Tianxiao 
                AU  - Xu, Gao 
                AU  - Golareh, Agha 
                AU  - Schwartz, Joel 
                AU  - Vokonas, Pantel 
                AU  - Just, Allan 
                AU  - Starr, John M. 
                AU  - McRae, Allan F. 
                AU  - Wray, Naomi R. 
                AU  - Visscher, Peter M. 
                AU  - Bressler, Jan 
                AU  - Zhang, Wen 
                AU  - Tanaka, Toshiko 
                AU  - Moore, Ann Zenobia 
                AU  - Pilling, Luke C. 
                AU  - Zhang, Guosheng 
                AU  - Stewart, James D. 
                AU  - Li, Yun 
                AU  - Hou, Lifang 
                AU  - Castillo-Fernandez, Juan 
                AU  - Spector, Tim 
                AU  - Kiel, Douglas P. 
                AU  - Murabito, Joanne M. 
                AU  - Liu, Chunyu 
                AU  - Mendelson, Mike 
                AU  - Assimes, Tim 
                AU  - Absher, Devin 
                AU  - Tsaho, Phil S. 
                AU  - Lu, Ake T. 
                AU  - Ferrucci, Luigi 
                AU  - Wilson, Rory 
                AU  - Waldenberger, Melanie 
                AU  - Prokisch, Holger 
                AU  - Bandinelli, Stefania 
                AU  - Bell, Jordana T. 
                AU  - Levy, Daniel 
                AU  - Deary, Ian J. 
                AU  - Horvath, Steve 
                AU  - Pankow, Jim 
                AU  - Peters, Annette 
                AU  - Whitsel, Eric A. 
                AU  - Baccarelli, Andrea 
                TI  - Blood DNA methylation sites predict death risk in a longitudinal study of 12, 300 individuals
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103408
                DO  - 10.18632/aging.103408
                SP  - 14092
                EP  - 14124
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Colicino, Elena 
                AU  - Marioni, Riccardo 
                AU  - Ward-Caviness, Cavin 
                AU  - Gondalia, Rahul 
                AU  - Guan, Weihua 
                AU  - Chen, Brian 
                AU  - Tsai, Pei-Chien 
                AU  - Huan, Tianxiao 
                AU  - Xu, Gao 
                AU  - Golareh, Agha 
                AU  - Schwartz, Joel 
                AU  - Vokonas, Pantel 
                AU  - Just, Allan 
                AU  - Starr, John M. 
                AU  - McRae, Allan F. 
                AU  - Wray, Naomi R. 
                AU  - Visscher, Peter M. 
                AU  - Bressler, Jan 
                AU  - Zhang, Wen 
                AU  - Tanaka, Toshiko 
                AU  - Moore, Ann Zenobia 
                AU  - Pilling, Luke C. 
                AU  - Zhang, Guosheng 
                AU  - Stewart, James D. 
                AU  - Li, Yun 
                AU  - Hou, Lifang 
                AU  - Castillo-Fernandez, Juan 
                AU  - Spector, Tim 
                AU  - Kiel, Douglas P. 
                AU  - Murabito, Joanne M. 
                AU  - Liu, Chunyu 
                AU  - Mendelson, Mike 
                AU  - Assimes, Tim 
                AU  - Absher, Devin 
                AU  - Tsaho, Phil S. 
                AU  - Lu, Ake T. 
                AU  - Ferrucci, Luigi 
                AU  - Wilson, Rory 
                AU  - Waldenberger, Melanie 
                AU  - Prokisch, Holger 
                AU  - Bandinelli, Stefania 
                AU  - Bell, Jordana T. 
                AU  - Levy, Daniel 
                AU  - Deary, Ian J. 
                AU  - Horvath, Steve 
                AU  - Pankow, Jim 
                AU  - Peters, Annette 
                AU  - Whitsel, Eric A. 
                AU  - Baccarelli, Andrea 
                TI  - Blood DNA methylation sites predict death risk in a longitudinal study of 12, 300 individuals
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103408
                DO  - 10.18632/aging.103408
                SP  - 14092
                EP  - 14124
                PY  - 
                AB  - DNA methylation has fundamental roles in gene programming and aging that may help predict mortality. However, no large-scale study has investigated whether site-specific DNA methylation predicts all-cause mortality. We used the Illumina-HumanMethylation450-BeadChip to identify blood DNA methylation sites associated with all-cause mortality for 12, 300 participants in 12 Cohorts of the Heart and Aging Research in Genetic Epidemiology (CHARGE) Consortium. Over an average 10-year follow-up, there were 2,561 deaths across the cohorts. Nine sites mapping to three intergenic and six gene-specific regions were associated with mortality (P &lt; 9.3x10-7) independently of age and other mortality predictors. Six sites (cg14866069, cg23666362, cg20045320, cg07839457, cg07677157, cg09615688)&#x2014;mapping respectively to BMPR1B, MIR1973, IFITM3, NLRC5, and two intergenic regions&#x2014;were associated with reduced mortality risk. The remaining three sites (cg17086398, cg12619262, cg18424841)&#x2014;mapping respectively to SERINC2, CHST12, and an intergenic region&#x2014;were associated with increased mortality risk. DNA methylation at each site predicted 5%&#x2013;15% of all deaths. We also assessed the causal association of those sites to age-related chronic diseases by using Mendelian randomization, identifying weak causal relationship between cg18424841 and cg09615688 with coronary heart disease. Of the nine sites, three (cg20045320, cg07839457, cg07677157) were associated with lower incidence of heart disease risk and two (cg20045320, cg07839457) with smoking and inflammation in prior CHARGE analyses. Methylation of cg20045320, cg07839457, and cg17086398 was associated with decreased expression of nearby genes (IFITM3, IRF, NLRC5, MT1, MT2, MARCKSL1) linked to immune responses and cardiometabolic diseases. These sites may serve as useful clinical tools for mortality risk assessment and preventative care.
                ER  -

Click to copy this citation from the text box above or download the citation:

The effect of Ganoderma lucidum spore oil in early skin wound healing: interactions of skin microbiota and inflammation

Chunwei Jiao, Yizhen Xie, Hao Yun, Huijia Liang, Chunyan He, Aimin Jiang, Qingping Wu, Burton B. Yang,

https://doi.org/10.18632/aging.103412 pp 14125—14140

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Jiao C, Xie Y, Yun H, Liang H, He C, Jiang A, Wu Q, Yang BB, . The effect of Ganoderma lucidum spore oil in early skin wound healing: interactions of skin microbiota and inflammation. . 12:14125-14140. https://doi.org/10.18632/aging.103412

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Jiao, Chunwei 
 AU - Xie, Yizhen 
 AU - Yun, Hao 
 AU - Liang, Huijia 
 AU - He, Chunyan 
 AU - Jiang, Aimin 
 AU - Wu, Qingping 
 AU - Yang, Burton B. 
 TI - The effect of Ganoderma lucidum spore oil in early skin wound healing: interactions of skin microbiota and inflammation
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103412
 DO - 10.18632/aging.103412
 SP - 14125
 EP - 14140
 PY - 
 AB - The mushroom Ganoderma lucidum (G. lucidum Leyss. ex Fr.) Karst has been a traditional Chinese medicine for millennia. In this study, we isolated the Ganoderma lucidum spore oil (GLSO) and evaluated the effect of GLSO on skin burn wound healing and the underlying mechanisms. Mice were used to perform skin wound healing assay. Wound analysis was performed by photography, hematoxylin/eosin staining, Masson&#x2019;s Trichrome staining and immunohistochemical analysis. Microbiota on the wounds were analyzed using the 16s rRNA sequence and quantitative statistics. The lipopolysaccharide (LPS) content was examined in skin wounds and serum using an enzyme-linked immunosorbent assay (ELISA). The expression of Toll-like receptor 4 (TLR4) and the relative levels of inflammatory cytokines were determined by qPCR and immunofluorescence assay. A pseudo-germfree mouse model treated with antibiotics was used to investigate whether GLSO accelerated skin burn wound healing through the skin microbiota. We found that GLSO significantly accelerated the process of skin wound healing and regulated the levels of gram-negative and gram-positive bacteria. Furthermore, GLSO reduced LPS and TLR4, and levels of some other related inflammatory cytokines. The assay with the pseudo-germfree mice model showed that GLSO had a significant acceleration on skin wound healing in comparison with antibiotic treatment. Thus, GLSO downregulated the inflammation by regulating skin microbiota to accelerate skin wound healing. These findings provide a scientific rationale for the potential therapeutic use of GLSO in skin burn injury.
 ER -

Click to copy this citation from the text box above or download the citation:

Long noncoding RNA AC092171.4 promotes hepatocellular carcinoma progression by sponging microRNA-1271 and upregulating GRB2

Chengjun Sun, Shanzhou Huang, Yuchen Hou, Zhongqiu Li, Dongmei Xia, Lishan Zhang, Yixi Zhang, Yifeng Cai, Ziming Wang, Qi Zhou, Xiaoshun He, Linwei Wu,

https://doi.org/10.18632/aging.103419 pp 14141—14156

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Sun C, Huang S, Hou Y, Li Z, Xia D, Zhang L, Zhang Y, Cai Y, Wang Z, Zhou Q, He X, Wu L, . Long noncoding RNA AC092171.4 promotes hepatocellular carcinoma progression by sponging microRNA-1271 and upregulating GRB2. . 12:14141-14156. https://doi.org/10.18632/aging.103419

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Sun, Chengjun 
                AU  - Huang, Shanzhou 
                AU  - Hou, Yuchen 
                AU  - Li, Zhongqiu 
                AU  - Xia, Dongmei 
                AU  - Zhang, Lishan 
                AU  - Zhang, Yixi 
                AU  - Cai, Yifeng 
                AU  - Wang, Ziming 
                AU  - Zhou, Qi 
                AU  - He, Xiaoshun 
                AU  - Wu, Linwei 
                TI  - Long noncoding RNA AC092171.4 promotes hepatocellular carcinoma progression by sponging microRNA-1271 and upregulating GRB2
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103419
                DO  - 10.18632/aging.103419
                SP  - 14141
                EP  - 14156
                PY  - 
                AB  - In this study, we investigated the mechanistic role of the long non-coding RNA (lncRNA) AC092171.4 in hepatocellular carcinoma (HCC). AC092171.4 was significantly upregulated in HCC tumor tissues compared to normal liver tissues. HCC patients with high AC092171.4 expression showed poorer overall survival (OS) and disease-free survival (DFS) than those with low AC092171.4 expression. In vitro cell proliferation, migration and invasiveness were all higher in AC092171.4-overexpressing HCC cells, but lower in AC092171.4-silenced HCC cells, than in controls. Balb/c nude mice injected with AC092171.4-silenced HCC cells had smaller xenograft tumors, which showed less growth and pulmonary metastasis than control tumors. Bioinformatics analyses and dual luciferase reporter assays confirmed that AC092171.4 binds directly to miR-1271, which targets the 3&#x2019;UTR of GRB2 mRNA. AC092171.4 expression correlates negatively with miR1271 expression and correlates positively with GRB2 mRNA expression in HCC tissues from patients. HCC cells co-transfected with miR-1271 mimics and sh-AC092171.4 show less proliferation, migration, invasiveness, GRB2 protein, and epithelial to mesencyhmal transition (EMT) than sh-AC092171.4-transfected HCC cells. These findings demonstrate that AC092171.4 promotes growth and progression of HCC by sponging miR-1271 and upregulating GRB2. This makes AC092171.4 a potential prognostic indicator and therapeutic target for HCC patients.
                ER  -

Click to copy this citation from the text box above or download the citation:

Circular RNA hsa_circ_0000073 contributes to osteosarcoma cell proliferation, migration, invasion and methotrexate resistance by sponging miR-145-5p and miR-151-3p and upregulating NRAS

Xia Li, Yi Liu, Xiangxin Zhang, Jun Shen, Renjie Xu, Yubo Liu, Xiao Yu,

https://doi.org/10.18632/aging.103423 pp 14157—14173

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li X, Liu Y, Zhang X, Shen J, Xu R, Liu Y, Yu X, . Circular RNA hsa_circ_0000073 contributes to osteosarcoma cell proliferation, migration, invasion and methotrexate resistance by sponging miR-145-5p and miR-151-3p and upregulating NRAS. . 12:14157-14173. https://doi.org/10.18632/aging.103423

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Xia 
                AU  - Liu, Yi 
                AU  - Zhang, Xiangxin 
                AU  - Shen, Jun 
                AU  - Xu, Renjie 
                AU  - Liu, Yubo 
                AU  - Yu, Xiao 
                TI  - Circular RNA hsa_circ_0000073 contributes to osteosarcoma cell proliferation, migration, invasion and methotrexate resistance by sponging miR-145-5p and miR-151-3p and upregulating NRAS
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103423
                DO  - 10.18632/aging.103423
                SP  - 14157
                EP  - 14173
                PY  - 
                AB  - An increasing number of studies have demonstrated that circular RNAs (circRNAs), as promising therapeutic targets, are essential for diverse human diseases, especially cancer. However, the potential functions and complex mechanisms of most circRNAs in osteosarcoma (OS) are still not fully elucidated. In the present study, we obtained the expression profile of circRNAs from a GEO database (GSE96964) and identified hsa_circ_0000073 as a highly expressed candidate in OS. Overexpression of hsa_circ_0000073 accelerated the proliferation, migration, invasion and MTX resistance of OS cells, and knockdown of hsa_circ_0000073 resulted in the opposite effects. Mechanistically, hsa_circ_0000073 upregulated NRAS expression by targeting miR-145-5p and miR-151-3p in OS cells. In addition, the promotion of OS progression by hsa_circ_000007 was blocked by miR-145-5p and miR-151-3p-mediated NRAS inhibition. In conclusion, hsa_circ_0000073 facilitated the proliferation, migration, invasion and MTX resistance of OS cells through the inhibition of miR-145-5p and miR-151-3p-mediated downregulation of NRAS.
                ER  -

Click to copy this citation from the text box above or download the citation:

LncRNA NEAT1/miR-129/Bcl-2 signaling axis contributes to HDAC inhibitor tolerance in nasopharyngeal cancer

Fei Xue, You Cheng, Li Xu, Chuan Tian, Hongye Jiao, Rui Wang, Xia Gao,

https://doi.org/10.18632/aging.103427 pp 14174—14188

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xue F, Cheng Y, Xu L, Tian C, Jiao H, Wang R, Gao X, . LncRNA NEAT1/miR-129/Bcl-2 signaling axis contributes to HDAC inhibitor tolerance in nasopharyngeal cancer. . 12:14174-14188. https://doi.org/10.18632/aging.103427

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xue, Fei 
                AU  - Cheng, You 
                AU  - Xu, Li 
                AU  - Tian, Chuan 
                AU  - Jiao, Hongye 
                AU  - Wang, Rui 
                AU  - Gao, Xia 
                TI  - LncRNA NEAT1/miR-129/Bcl-2 signaling axis contributes to HDAC inhibitor tolerance in nasopharyngeal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103427
                DO  - 10.18632/aging.103427
                SP  - 14174
                EP  - 14188
                PY  - 
                AB  - Histone deacetylase inhibitors (HDACis) - based therapeutic drug tolerance is one of the principal factors of poor prognosis of patients with nasopharyngeal cancer (NPC). Mechanisms of tolerance to HDACis are not well understood. Nowadays, dysregulation of long non-coding RNAs (LncRNAs) and microRNAs (miRNAs) has been reported to provide beneficial or inhibitory effects in drug-tolerance in various cancers. Herein, we established the HDAC inhibitor (SAHA)-tolerant NPC cell sublines, which had decreased apoptosis in response to SAHA treatment. We observed that the expression of miR-129 was significantly reduced in SAHA-tolerant NPC cells. Manipulating the expression of miR-129 overcame SAHA tolerance, and enhanced the SAHA-induced apoptosis. In terms of miR-129 downregulation, we identified that NEAT1 suppresses miR-129 expression. NEAT1 was found to be upregulated in SAHA tolerance cells. The depletion of NEAT1 phenocopied the effect of miR-129 overexpression, which also enhanced SAHA-induced apoptosis. Bcl-2 was the downstream target of miR-129 and contributed to SAHA tolerance in NPC. Our in vivo xenograft experiment confirmed that the administration of miR-129 or inhibition of Bcl-2 overcame the SAHA tolerance in NPC. In conclusion, NEAT1 increases in NPC tissues and manages to facilitate SAHA tolerance by modulating the miR-129/Bcl-2 axis, providing novel therapeutic targets for NPC treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Co-exposure to multi-walled carbon nanotube and lead ions aggravates hepatotoxicity of nonalcoholic fatty liver via inhibiting AMPK/PPARγ pathway

Enqin Liu, Xinghui Wang, Xidong Li, Ping Tian, Hao Xu, Zenglian Li, Likun Wang,

https://doi.org/10.18632/aging.103430 pp 14189—14204

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liu E, Wang X, Li X, Tian P, Xu H, Li Z, Wang L, . Co-exposure to multi-walled carbon nanotube and lead ions aggravates hepatotoxicity of nonalcoholic fatty liver via inhibiting AMPK/PPARγ pathway. . 12:14189-14204. https://doi.org/10.18632/aging.103430

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liu, Enqin 
                AU  - Wang, Xinghui 
                AU  - Li, Xidong 
                AU  - Tian, Ping 
                AU  - Xu, Hao 
                AU  - Li, Zenglian 
                AU  - Wang, Likun 
                TI  - Co-exposure to multi-walled carbon nanotube and lead ions aggravates hepatotoxicity of nonalcoholic fatty liver via inhibiting AMPK/PPARγ pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103430
                DO  - 10.18632/aging.103430
                SP  - 14189
                EP  - 14204
                PY  - 
                AB  - Multi-walled carbon nanotubes (MWCNTs) have been widely used in sewage disposal, water purification, and disinfection. Co-exposure to MWCNTs and heavy metal ions is common during water disposal. However, the hepatotoxicity of co-exposure to MWCNTs and lead ions for nonalcoholic fatty liver disease (NAFLD) subjects has not been investigated. NAFLD mice were fed intragastrically with MWCNTs and lead acetate (PbAc). Combined administration of MWCNTs and PbAc significantly damaged the liver function, and aggravated the nonalcoholic steatohepatitis phenotype as well as the hepatic fibrosis and steatosis in NAFLD mice. Furthermore, MWCNTs and PbAc significantly induced apoptosis in primary hepatocytes isolated from NAFLD mice. Combined administration of MWCNTs and PbAc also resulted in hepatic lipid peroxidation by inducing antioxidant defense system dysfunction, and significantly enhanced the expression levels of inflammatory cytokines in NAFLD mice livers. Meanwhile, combined administration of MWCNTs and PbAc may exert its hepatotoxicity in the NAFLD via inhibiting the adenosine 5&#x2018;-monophosphate activated protein kinase (AMPK)/peroxisome proliferator-activated receptors &#x3B3; (PPAR&#x3B3;) pathway. Taken together, we conclude that co-exposure to MWCNTs and PbAc can remarkably aggravate the hepatotoxicity in NAFLD mice via inhibiting the AMPK/PPAR&#x3B3; pathway. This study may provide a biosafety evaluation for the application of nanomaterials in wastewater treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Lowered levels of nicotinic acetylcholine receptors and elevated apoptosis in the hippocampus of brains from patients with type 2 diabetes mellitus and db/db mice

Yi Xu, Kun Cao, Bing Guo, Jie Xiang, Yang-Ting Dong, Xiao-Lan Qi, Wen-Feng Yu, Yan Xiao, Zhi-Zhong Guan,

https://doi.org/10.18632/aging.103435 pp 14205—14218

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu Y, Cao K, Guo B, Xiang J, Dong Y, Qi X, Yu W, Xiao Y, Guan Z, . Lowered levels of nicotinic acetylcholine receptors and elevated apoptosis in the hippocampus of brains from patients with type 2 diabetes mellitus and db/db mice. . 12:14205-14218. https://doi.org/10.18632/aging.103435

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Xu, Yi 
 AU - Cao, Kun 
 AU - Guo, Bing 
 AU - Xiang, Jie 
 AU - Dong, Yang-Ting 
 AU - Qi, Xiao-Lan 
 AU - Yu, Wen-Feng 
 AU - Xiao, Yan 
 AU - Guan, Zhi-Zhong 
 TI - Lowered levels of nicotinic acetylcholine receptors and elevated apoptosis in the hippocampus of brains from patients with type 2 diabetes mellitus and db/db mice
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103435
 DO - 10.18632/aging.103435
 SP - 14205
 EP - 14218
 PY - 
 AB - Cognitive impairment caused by diabetes has been gradually recognized. Generally, nicotinic acetylcholine receptors (nAChRs) play an important role in the pathogenesis in dementia disorders including Alzheimer&apos;s disease (AD). However, the expression of nAChRs in the brains of type 2 diabetes mellitus (T2DM) is unexplored. This study explored the alterations of nAChRs in the postmortem brains of patients with T2DM and brains of db/db mice. Morris water maze test was used to appraise the ability of spatial learning and memory; Western blotting and RT-qPCR were performed to determine the expressions of target protein and mRNA, respectively; TUNEL was used to detect the apoptosis of neurons. We found that the protein levels of nAChR &#x3B1;7 and &#x3B1;4 subunits were significantly decreased and the apoptosis rates in neurons elevated in the hippocampus of T2DM patients and db/db mice as comparison to controls. Furthermore, the db/db mice exhibited the impaired cognition, the elevated level of pro-apoptotic protein and the reduced level of anti-apoptotic and synaptic proteins. This study shows the lowered level of nAChR &#x3B1;7 and &#x3B1;4 subunits and the elevated apoptosis in the hippocampus of T2DM patients and db/db mice, which might help explain the impaired cognition in T2DM.
 ER -

Click to copy this citation from the text box above or download the citation:

Decreased lncRNA, TINCR, promotes growth of colorectal carcinoma through upregulating microRNA-31

Zhong Ren, Jingzheng Liu, Jian Li, Liqing Yao,

https://doi.org/10.18632/aging.103436 pp 14219—14231

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ren Z, Liu J, Li J, Yao L, . Decreased lncRNA, TINCR, promotes growth of colorectal carcinoma through upregulating microRNA-31. . 12:14219-14231. https://doi.org/10.18632/aging.103436

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ren, Zhong 
                AU  - Liu, Jingzheng 
                AU  - Li, Jian 
                AU  - Yao, Liqing 
                TI  - Decreased lncRNA, TINCR, promotes growth of colorectal carcinoma through upregulating microRNA-31
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103436
                DO  - 10.18632/aging.103436
                SP  - 14219
                EP  - 14231
                PY  - 
                AB  - Abnormal expression in terminal differentiation-induced noncoding RNA (TINCR), a long non-coding RNA (lncRNA), has been reported in different human cancers, including colorectal carcinoma (CRC). Moreover, the molecular mechanisms that underlie the effects of TINCR on CRC remain unclear. Here, by a set of bioinformatics studies, we found that microRNA-31 (miR-31), the oncogenic miRNA that robustly upregulates in CRC, was a sponge miRNA for TINCR. TINCR and miR-31 levels were inversely correlated in both CRC tissues and CRC cell lines. Luciferase reporter assay revealed a specific binding site on TINCR for miR-31. Suppression of TINCR promoted CRC cell growth and migration in vitro, while overexpression of TINCR inhibited CRC cell growth and migration in vitro. TINCR depletion increased tumor xenograft growth in vivo, while TINCR overexpression inhibited it. Together, our study suggests that re-expressing TINCR may suppress invasive outgrowth of CRC through miR-31.
                ER  -

Click to copy this citation from the text box above or download the citation:

Minocycline inhibition of microglial rescues nigrostriatal dopaminergic neurodegeneration caused by mutant alpha-synuclein overexpression

Yong Wang, Qian Wang, Ruobing Yu, Qi Zhang, Zhonghai Zhang, Haiying Li, Chao Ren, Rongli Yang, Haichen Niu,

https://doi.org/10.18632/aging.103440 pp 14232—14243

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang Y, Wang Q, Yu R, Zhang Q, Zhang Z, Li H, Ren C, Yang R, Niu H, . Minocycline inhibition of microglial rescues nigrostriatal dopaminergic neurodegeneration caused by mutant alpha-synuclein overexpression. . 12:14232-14243. https://doi.org/10.18632/aging.103440

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Yong 
                AU  - Wang, Qian 
                AU  - Yu, Ruobing 
                AU  - Zhang, Qi 
                AU  - Zhang, Zhonghai 
                AU  - Li, Haiying 
                AU  - Ren, Chao 
                AU  - Yang, Rongli 
                AU  - Niu, Haichen 
                TI  - Minocycline inhibition of microglial rescues nigrostriatal dopaminergic neurodegeneration caused by mutant alpha-synuclein overexpression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103440
                DO  - 10.18632/aging.103440
                SP  - 14232
                EP  - 14243
                PY  - 
                AB  - Studies indicate that mutant &#x3B1;-synuclein (m&#x3B1;Syn) is involved in the pathogenesis of Parkinson&#x2019;s disease (PD). The m&#x3B1;Syn expression leads to the loss of dopaminergic neurons in the substantia nigra (SN) and consequent motor dysfunctions. Additionally, studies found that PD was accompanied by extensive neuroinflammation of SN. However, it remains unclear as to whether microglia participate in the m&#x3B1;Syn pathology. This issue is addressed by using AAV-m&#x3B1;-Syn (A30P-A53T) to overexpress the human m&#x3B1;Syn in the SN in view of establishing the PD model. Subsequently, minocycline (Mino) was used to inhibit microglia activity, and an interleukin-1 receptor (IL-1R1) antagonist was used to hinder the IL-1R1 function. Finally, immunohistochemistry was used to analyze phosphorylated &#x3B1;Syn (Ser129) and TH-positive cells in the SN. Dopamine levels were analyzed by high performance liquid chromatography. m&#x3B1;Syn overexpression in the SN induced motor dysfunction, decreased striatal dopamine levels, and increased pathological &#x3B1;Syn 12 weeks after AAV injection. The data demonstrated that inhibiting microglial activation or hindering IL-1R1 reversed the persistent motor deficits, neurodegeneration of the nigrostriatal dopaminergic system, and development of Lewy body pathology caused by human m&#x3B1;Syn overexpression in the SN. Additionally, these findings indicate that neuroinflammation promotes the loss of neuronal cells.
                ER  -

Click to copy this citation from the text box above or download the citation:

Efficacy and safety of therapies for EGFR-mutant non-small cell lung cancer with brain metastasis: an evidence-based Bayesian network pooled study of multivariable survival analyses

Binghao Zhao, Yuekun Wang, Yaning Wang, Wenlin Chen, Lizhou Zhou, Peng Hao Liu, Ziren Kong, Congxin Dai, Yu Wang, Wenbin Ma,

https://doi.org/10.18632/aging.103455 pp 14244—14270

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhao B, Wang Y, Wang Y, Chen W, Zhou L, Liu PH, Kong Z, Dai C, Wang Y, Ma W, . Efficacy and safety of therapies for EGFR-mutant non-small cell lung cancer with brain metastasis: an evidence-based Bayesian network pooled study of multivariable survival analyses. . 12:14244-14270. https://doi.org/10.18632/aging.103455

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhao, Binghao 
                AU  - Wang, Yuekun 
                AU  - Wang, Yaning 
                AU  - Chen, Wenlin 
                AU  - Zhou, Lizhou 
                AU  - Liu, Peng Hao 
                AU  - Kong, Ziren 
                AU  - Dai, Congxin 
                AU  - Wang, Yu 
                AU  - Ma, Wenbin 
                TI  - Efficacy and safety of therapies for EGFR-mutant non-small cell lung cancer with brain metastasis: an evidence-based Bayesian network pooled study of multivariable survival analyses
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103455
                DO  - 10.18632/aging.103455
                SP  - 14244
                EP  - 14270
                PY  - 
                AB  - Preferable treatments for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) with brain metastasis are elusive. The study intended to estimate the relative efficacy and safety of systemic therapies. Clinical trials about therapies for EGFR-mutant, brain-metastatic NSCLC were identified. Progression-free survival (PFS) and overall survival (OS) were analysed using random effects Bayesian network meta-analyses (NMAs) on the hazard ratio (HR)-scale. Nomogram and Kaplan-Meier plots based on clinical or individual factors are displayed using data obtained from the Surveillance Epidemiology and End Results (SEER) database. Third-generation EGFR- tyrosine kinase inhibitors (EGFR-TKI) (osimertinib), EGFR-TKIs + stereotactic radiosurgery (SRS)/whole brain radiotherapy (WBRT) (gefitinib/erlotinib + SRS/WBRT), and EGFR-TKIs (erlotinib) + anti-vascular endothelial growth factor receptor (anti-VEGFR) (bevacizumab) achieved superior PFS (HR: 0.30 (0.15-0.59); HR: 0.47 (0.31-0.72); HR: 0.50 (0.21-1.21) vs. deferring SRS/WBRT) and acceptability; EGFR-TKIs + SRS/WBRT was top ranking (vs. others) for OS followed by third-generation EGFR-TKI. In the dataset cohort of 1173 brain-metastatic NSCLC patients, the 6-month, 1-year, and 3-year survival rates were 59.8%, 41.3%, and 5.6%, respectively. Race and origin, and year of diagnosis were independent predictors of OS. Survival curves showed that the OS of patients varied significantly by histology and race. Third-generation EGFR-TKI and EGFR-TKIs + SRS/WBRT are more effective and potentially acceptable for EGFR-mutant NSCLC with brain metastases balancing OS and PFS. Surgeries without adjuvant therapies cannot significantly improve the OS of brain-metastatic NSCLC patients. The study highlights importance of osimertinib in these patients and provide a reference for clinical treatments.
                ER  -

Click to copy this citation from the text box above or download the citation:

Analysis of the expression and genetic alteration of CLDN18 in gastric cancer

Jian Li, Yao Zhang, Dengmin Hu, Tuping Gong, Run Xu, Jun Gao,

https://doi.org/10.18632/aging.103457 pp 14271—14284

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li J, Zhang Y, Hu D, Gong T, Xu R, Gao J, . Analysis of the expression and genetic alteration of CLDN18 in gastric cancer. . 12:14271-14284. https://doi.org/10.18632/aging.103457

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Jian 
                AU  - Zhang, Yao 
                AU  - Hu, Dengmin 
                AU  - Gong, Tuping 
                AU  - Xu, Run 
                AU  - Gao, Jun 
                TI  - Analysis of the expression and genetic alteration of CLDN18 in gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103457
                DO  - 10.18632/aging.103457
                SP  - 14271
                EP  - 14284
                PY  - 
                AB  - Claudin 18 (CLDN18) is a transmembrane protein that localizes to apical regions to form tight junction complexes. Abnormal expression of CLDN18 has been reported in gastric cancer (GC). The expression, genetic alterations, and prognostic role of CLDN18 were analyzed using public data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Human Protein Atlas (HPA) databases using multiple online tools. The biological network of CLDN18 was determined using GeneMANIA. Expression of CLDN18 was restricted to lung and stomach in normal tissues, was significantly downregulated in GC, but was ectopically overexpressed in some other cancer types. There was no correlation between mRNA expression of CLDN18 and the clinicopathology of GC, although expression was higher in the Epstein-Barr virus (EBV)-positive subgroup than other subgroups. Genetic alteration of CLDN18 was not a common event in GC; the main alteration was gene fusion with ARHGAP26. CLDN18 expression did not predict the overall survival (OS) of GC patients. This study summarizes the expression features of CLDN18 in GC and suggests it may serve as a biomarker and therapy target for GC.
                ER  -

Click to copy this citation from the text box above or download the citation:

C5aR deficiency attenuates the breast cancer development via the p38/p21 axis

Jian Chen, Zi-han Sun, Li-ying Chen, Feng Xu, Yun-pei Zhao, Gui-qing Li, Ming Tang, You Li, Quan-you Zheng, Shu-feng Wang, Xin-hua Yang, Yu-zhang Wu, Gui-lian Xu,

https://doi.org/10.18632/aging.103468 pp 14285—14299

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen J, Sun Z, Chen L, Xu F, Zhao Y, Li G, Tang M, Li Y, Zheng Q, Wang S, Yang X, Wu Y, Xu G, . C5aR deficiency attenuates the breast cancer development via the p38/p21 axis. . 12:14285-14299. https://doi.org/10.18632/aging.103468

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Jian 
                AU  - Sun, Zi-han 
                AU  - Chen, Li-ying 
                AU  - Xu, Feng 
                AU  - Zhao, Yun-pei 
                AU  - Li, Gui-qing 
                AU  - Tang, Ming 
                AU  - Li, You 
                AU  - Zheng, Quan-you 
                AU  - Wang, Shu-feng 
                AU  - Yang, Xin-hua 
                AU  - Wu, Yu-zhang 
                AU  - Xu, Gui-lian 
                TI  - C5aR deficiency attenuates the breast cancer development via the p38/p21 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103468
                DO  - 10.18632/aging.103468
                SP  - 14285
                EP  - 14299
                PY  - 
                AB  - Emerging evidence has shown activation of the complement component C5 to C5a in cancer tissues and C5aR expression in breast cancer cells relates to the tumor development and poor prognosis, suggesting the involvement of complement C5a/C5aR pathway in the breast cancer pathogenesis. In this study, we found that as compared to the non-tumoral tissues, both C5aR and MAPK/p38 showed an elevated expression, but p21/p-p21 showed lower expression, in the tumoral tissues of breast cancer patients. Mice deficient in C5aR or mice treated with the C5aR antagonist exhibited attenuation of breast cancer growth and reduction in the p38/p-p38 expression, but increase in p21/p-p21 expression, in the tumor tissues. Pre-treatment of the breast cancer cells with recombinant C5a resulted in reduced p21 expression, and MAPK/p38 inhibitors prevented C5a-induced reduction in p21 expression, suggesting the involvement of the MAPK/p38 signaling pathway in the C5a/C5aR-mediated suppression of p21/p-p21 expression. These results provide evidence that breast cancer development may rely on C5a/C5aR interaction, for which MAPK/p38 pathway participate in down-regulating the p21 expression. Inhibition of C5a/C5aR pathway is expected to be helpful for the treatment of patients with breast cancer.
                ER  -

Click to copy this citation from the text box above or download the citation:

Caveolin-3 protects diabetic hearts from acute myocardial infarction/reperfusion injury through β2AR, cAMP/PKA, and BDNF/TrkB signaling pathways

Jiaji Gong, Fan Zhou, Simin Xie, Xin Wang, Junmei Xu, Feng Xiao,

https://doi.org/10.18632/aging.103469 pp 14300—14313

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gong J, Zhou F, Xie S, Wang X, Xu J, Xiao F, . Caveolin-3 protects diabetic hearts from acute myocardial infarction/reperfusion injury through β2AR, cAMP/PKA, and BDNF/TrkB signaling pathways. . 12:14300-14313. https://doi.org/10.18632/aging.103469

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gong, Jiaji 
                AU  - Zhou, Fan 
                AU  - Xie, Simin 
                AU  - Wang, Xin 
                AU  - Xu, Junmei 
                AU  - Xiao, Feng 
                TI  - Caveolin-3 protects diabetic hearts from acute myocardial infarction/reperfusion injury through β2AR, cAMP/PKA, and BDNF/TrkB signaling pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103469
                DO  - 10.18632/aging.103469
                SP  - 14300
                EP  - 14313
                PY  - 
                AB  - Diabetes mellitus (DM) might increase the incidence and mortality of cardiac failure after acute myocardial infarction (AMI) in patients. We attempted to investigate whether Caveolin-3 showed beneficial effects in DM patient post-MI injury through the cAMP/PKA and BDNF/TrkB signaling pathways. The activity of ADRB2 and cAMP/PKA signaling were impaired in nondiabetic ischemia-reperfusion (I/R) group compared with the sham and DM groups and were more impaired in diabetic I/R group than in the I/R group. In H9C2 cells, high-glucose (HG) stimulation further enhanced H/R injury by promoting cell apoptosis, inhibiting cell viability, and suppressing TrkB and Akt signaling; in contrast, the ADRB2 agonist isoprenaline (ISO) significantly attenuated the above-described effects of HG stimulation. Caveolin-3 overexpression promoted the localization of ADRB2 on the membrane of the HG-stimulated H9C2 cells, subsequently inhibiting apoptosis and promoting cell viability. Under HG stimulation, Caveolin-3 overexpression enhanced the activity of the cAMP/PKA and BDNF/TrkB signaling pathways, whereas ADRB2 silencing reversed the effects of Caveolin-3 overexpression. In conclusion, ADRB2 agonist promoted the activity of the BDNF/TrkB and cAMP/PKA signaling pathways, mitigating the HG-aggravated H/R injuries in H9C2 cells. Caveolin-3 exerts a protective effect on diabetic hearts against I/R damage through the &#x3B2;2AR, cAMP/PKA, and BDNF/TrkB signaling pathways.
                ER  -

Click to copy this citation from the text box above or download the citation:

Circular RNA-9119 suppresses in ovarian cancer cell viability via targeting the microRNA-21-5p–PTEN–Akt pathway

Jianming Gong, Xiaoyang Xu, Xuanli Zhang, Yingqiao Zhou,

https://doi.org/10.18632/aging.103470 pp 14314—14328

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gong J, Xu X, Zhang X, Zhou Y, . Circular RNA-9119 suppresses in ovarian cancer cell viability via targeting the microRNA-21-5p–PTEN–Akt pathway. . 12:14314-14328. https://doi.org/10.18632/aging.103470

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gong, Jianming 
                AU  - Xu, Xiaoyang 
                AU  - Zhang, Xuanli 
                AU  - Zhou, Yingqiao 
                TI  - Circular RNA-9119 suppresses in ovarian cancer cell viability via targeting the microRNA-21-5p–PTEN–Akt pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103470
                DO  - 10.18632/aging.103470
                SP  - 14314
                EP  - 14328
                PY  - 
                AB  - We aimed to assess the regulatory role of circular RNA (circRNA)-9119 (circ9119) in ovarian cancer (OC) cell viability. The expression of circ9119 was clearly reduced in OC tissues and cell lines, whereas the microRNA-21-5p (miR-21) levels were elevated compared with those in normal healthy control tissues and immortalized fallopian epithelial cell line FTE187. Further, circ9119 was overexpressed, causing a notable decrease in the viability and proliferation of OC cells and an increase in apoptosis. Further study showed that circ9119 upregulation resulted in a decrease in miR-21 levels. Bioinformatics forecasting (starBase and TargetScan) and dual luciferase reporter assay demonstrated that circ9119 acts as an miR-21 sponge. Recovery of miR-21 expression in circ9119-overexpressing OC cells showed that miR-21 exhibited the opposite effect on circ9119; moreover, its recovery could suppress the effects of circ9119 overexpression, recover cell proliferation, and reduce apoptosis. Furthermore, miR-21 was found to target phosphatase and tensin homologue (PTEN) 3&#x2032; untranslated region. PTEN protein and mRNA expression was reduced in OC tissues and cells, whereas it was increased on transfection with an miR-21 inhibitor. Thus, circ9119 could regulate cell proliferation and apoptosis of OC cells via by acting as an miR-21 sponge and targeting the PTEN&#x2013;Akt pathway.
                ER  -

Click to copy this citation from the text box above or download the citation:

Downregulation of hsa_circ_0007580 inhibits non-small cell lung cancer tumorigenesis by reducing miR-545-3p sponging

Shuifang Chen, Shan Lu, Yinan Yao, Junjun Chen, Guangdie Yang, Lingfang Tu, Zeying Zhang, Jianli Zhang, Lina Chen,

https://doi.org/10.18632/aging.103472 pp 14329—14340

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen S, Lu S, Yao Y, Chen J, Yang G, Tu L, Zhang Z, Zhang J, Chen L, . Downregulation of hsa_circ_0007580 inhibits non-small cell lung cancer tumorigenesis by reducing miR-545-3p sponging. . 12:14329-14340. https://doi.org/10.18632/aging.103472

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Shuifang 
                AU  - Lu, Shan 
                AU  - Yao, Yinan 
                AU  - Chen, Junjun 
                AU  - Yang, Guangdie 
                AU  - Tu, Lingfang 
                AU  - Zhang, Zeying 
                AU  - Zhang, Jianli 
                AU  - Chen, Lina 
                TI  - Downregulation of hsa_circ_0007580 inhibits non-small cell lung cancer tumorigenesis by reducing miR-545-3p sponging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103472
                DO  - 10.18632/aging.103472
                SP  - 14329
                EP  - 14340
                PY  - 
                AB  - Non-small cell lung cancer (NSCLC) is a highly malignant tumor. Many circular RNAs (circRNAs) are reportedly in regulating the progression of NSCLC. To identify potential therapeutic targets for NSCLC, we conducted a bioinformatics analysis of circRNAs differentially expressed between NSCLC tissues and adjacent normal tissues. Hsa_circ_0007580 was upregulated in NSCLC tumor tissues, and the expression of its host gene (protein kinase Ca) correlated negatively with overall survival. Short-hairpin RNAs were used to knock down hsa_circ_0007580 in NSCLC cells, and gene and protein levels were measured with qRT-PCR and Western blotting, respectively. NSCLC cell proliferation, migration and apoptosis were evaluated with CCK-8 assays, Ki-67 staining, Transwell assays and flow cytometry, respectively. Knocking down hsa_circ_0007580 inhibited proliferation and invasion by NSCLC cells and induced their apoptosis. Dual luciferase reporter assays indicated that miR-545-3p can bind to hsa_circ_0007580 (suggesting that hsa_circ_0007580 sponges miR-545-3p) and to protein kinase Ca (suggesting that miR-545-3p directly inhibits this gene). In a xenograft tumor model, downregulating hsa_circ_0007580 inhibited NSCLC tumorigenesis by inactivating p38/mitogen-activated protein kinase signaling. Thus, silencing hsa_circ_0007580 notably inhibited NSCLC progression in vitro and in vivo, suggesting this circRNA could be a novel treatment target for NSCLC.
                ER  -

Click to copy this citation from the text box above or download the citation:

LKB1 inactivation leads to centromere defects and genome instability via p53-dependent upregulation of survivin

Li-Yan Jin, Kui Zhao, Long-Jiang Xu, Rui-Xun Zhao, Kaitlin D. Werle, Yong Wang, Xiao-Long Liu, Qiu Chen, Zhuo-Jun Wu, Ke Zhang, Ying Zhao, Guo-Qin Jiang, Feng-Mei Cui, Zhi-Xiang Xu,

https://doi.org/10.18632/aging.103473 pp 14341—14354

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Jin L, Zhao K, Xu L, Zhao R, Werle KD, Wang Y, Liu X, Chen Q, Wu Z, Zhang K, Zhao Y, Jiang G, Cui F, et al, . LKB1 inactivation leads to centromere defects and genome instability via p53-dependent upregulation of survivin. . 12:14341-14354. https://doi.org/10.18632/aging.103473

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Jin, Li-Yan 
                AU  - Zhao, Kui 
                AU  - Xu, Long-Jiang 
                AU  - Zhao, Rui-Xun 
                AU  - Werle, Kaitlin D. 
                AU  - Wang, Yong 
                AU  - Liu, Xiao-Long 
                AU  - Chen, Qiu 
                AU  - Wu, Zhuo-Jun 
                AU  - Zhang, Ke 
                AU  - Zhao, Ying 
                AU  - Jiang, Guo-Qin 
                AU  - Cui, Feng-Mei 
                AU  - Xu, Zhi-Xiang 
                TI  - LKB1 inactivation leads to centromere defects and genome instability via p53-dependent upregulation of survivin
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103473
                DO  - 10.18632/aging.103473
                SP  - 14341
                EP  - 14354
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Jin, Li-Yan 
                AU  - Zhao, Kui 
                AU  - Xu, Long-Jiang 
                AU  - Zhao, Rui-Xun 
                AU  - Werle, Kaitlin D. 
                AU  - Wang, Yong 
                AU  - Liu, Xiao-Long 
                AU  - Chen, Qiu 
                AU  - Wu, Zhuo-Jun 
                AU  - Zhang, Ke 
                AU  - Zhao, Ying 
                AU  - Jiang, Guo-Qin 
                AU  - Cui, Feng-Mei 
                AU  - Xu, Zhi-Xiang 
                TI  - LKB1 inactivation leads to centromere defects and genome instability via p53-dependent upregulation of survivin
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103473
                DO  - 10.18632/aging.103473
                SP  - 14341
                EP  - 14354
                PY  - 
                AB  - Inactivating mutations in the liver kinase B1 (LKB1) tumor suppressor gene underlie Peutz-Jeghers syndrome (PJS) and occur frequently in various human cancers. We previously showed that LKB1 regulates centrosome duplication via PLK1. Here, we report that LKB1 further helps to maintain genomic stability through negative regulation of survivin, a member of the chromosomal passenger complex (CPC) that mediates CPC targeting to the centromere. We found that loss of LKB1 led to accumulation of misaligned and lagging chromosomes at metaphase and anaphase and increased the appearance of multi- and micro-nucleated cells. Ectopic LKB1 expression reduced these features and improved mitotic fidelity in LKB1-deficient cells. Through pharmacological and genetic manipulations, we showed that LKB1-mediated repression of survivin is independent of AMPK, but requires p53. Consistent with the key influence of LKB1 on survivin expression, immunohistochemical analysis indicated that survivin is highly expressed in intestinal polyps from a PJS patient. Lastly, we reaffirm a potential therapeutic avenue to treat LKB1-mutated tumors by demonstrating the increased sensitivity to survivin inhibitors of LKB1-deficient cells.
                ER  -

Click to copy this citation from the text box above or download the citation:

LncRNA FGD5-AS1 promotes tumor growth by regulating MCL1 via sponging miR-153-3p in oral cancer

Chao Ge, Jiali Dong, Yahui Chu, Sumin Cao, Jing Zhang, Jianming Wei,

https://doi.org/10.18632/aging.103476 pp 14355—14364

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ge C, Dong J, Chu Y, Cao S, Zhang J, Wei J, . LncRNA FGD5-AS1 promotes tumor growth by regulating MCL1 via sponging miR-153-3p in oral cancer. . 12:14355-14364. https://doi.org/10.18632/aging.103476

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ge, Chao 
                AU  - Dong, Jiali 
                AU  - Chu, Yahui 
                AU  - Cao, Sumin 
                AU  - Zhang, Jing 
                AU  - Wei, Jianming 
                TI  - LncRNA FGD5-AS1 promotes tumor growth by regulating MCL1 via sponging miR-153-3p in oral cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103476
                DO  - 10.18632/aging.103476
                SP  - 14355
                EP  - 14364
                PY  - 
                AB  - Purpose: To investigate the function of long noncoding RNA (lncRNA) FGD5-AS1 in oral cancer (OC) and to further clarify the regulation of FGD5-AS1 on miR-153-3p/MCL1 axis.Results: FGD5-AS1 was significantly increased in OC tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of OC cells. FGD5-AS1 acted as a sponge of miR-153-3p, and MCL1 was direct target of miR-153-3p. Forced expression of miR-153-3p or inhibition of MCL1 reversed the promoted role of FGD5-AS1 on OC cells&#x2019; migration and invasion. The in vivo tumor growth assay showed that FGD5-AS1 promoted OC tumorigenesis by regulating miR-153-3p/MCL1 axis.Conclusions: Our research revealed lncRNA FGD5-AS1 acted as an oncogene by regulating MCL1 via sponging miR-153-3p, thus providing some novel experimental basis for clinical treatment or prevention of OC.Patients and Methods: The mRNA expression of FGD5-AS1, miR-153-3p and MCL1 was detected by qRT-PCR. CCK8 assay, Edu assay, wound healing assay and transwell assay were used to detect the FGD5-AS1/ miR-153-3p/MCL1 axis function on proliferation, migration and invasion in OC cells. Western blot was used to calculate protein level of MCL1. Luciferase assay was used to detect the binding of miR-153-3p and MCL1, FGD5-AS1and miR-153-3p.
                ER  -

Click to copy this citation from the text box above or download the citation:

Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis

Hua Wei, Cong Cao, Xiaojuan Wei, Minglv Meng, Biaoliang Wu, Lianxin Meng, Xi Wei, Shixing Gu, Hongmian Li,

https://doi.org/10.18632/aging.103478 pp 14365—14375

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wei H, Cao C, Wei X, Meng M, Wu B, Meng L, Wei X, Gu S, Li H, . Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis. . 12:14365-14375. https://doi.org/10.18632/aging.103478

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wei, Hua 
                AU  - Cao, Cong 
                AU  - Wei, Xiaojuan 
                AU  - Meng, Minglv 
                AU  - Wu, Biaoliang 
                AU  - Meng, Lianxin 
                AU  - Wei, Xi 
                AU  - Gu, Shixing 
                AU  - Li, Hongmian 
                TI  - Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103478
                DO  - 10.18632/aging.103478
                SP  - 14365
                EP  - 14375
                PY  - 
                AB  - More and more findings illustrate the critical roles of circular RNA (circRNA) in diabetes mellitus (DM) and its complications. A major pathological characteristic for DM is the apoptosis of endothelial cells (ECs) induced by high glucose (HG), however, the function of circRNA in the ECs&#x2019; phenotypes is still elusive. Here, this study identified an up-regulated circRNA (circVEGFC) in the HG-induced human umbilical vein endothelial cells (HUVECs). Functionally, knockdown of circVEGFC alleviated the apoptosis and recovered the proliferation in HUVECs induced by HG administration. Mechanistically, circVEGFC functioned as the sponge of miR-338-3p, and miR-338-3p was found to target the 3&#x2019;-Untranslated Regions (3&#x2019;-UTR) of hypoxia inducible factor 1 alpha (HIF-1&#x3B1;). HIF-1&#x3B1;, a critical transcription factor in DM, could activate the transcription of vascular endothelial growth factor A (VEGFA) and promote its protein product. In conclusion, these findings reveal the promotion of circVEGFC/miR-338-3p/HIF-1&#x3B1;/VEGFA axis in the HG-induced ECs&#x2019; apoptosis, providing a potential treatment strategy for ECs&#x2019; damage in DM.
                ER  -

Click to copy this citation from the text box above or download the citation:

MicroRNA-15a/16/SOX5 axis promotes migration, invasion and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes

Hua Wei, Qin Wu, Yumeng Shi, Aishu Luo, Shiyu Lin, Xiaoke Feng, Jintao Jiang, Miaojia Zhang, Fang Wang, Wenfeng Tan,

https://doi.org/10.18632/aging.103480 pp 14376—14390

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wei H, Wu Q, Shi Y, Luo A, Lin S, Feng X, Jiang J, Zhang M, Wang F, Tan W, . MicroRNA-15a/16/SOX5 axis promotes migration, invasion and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes. . 12:14376-14390. https://doi.org/10.18632/aging.103480

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wei, Hua 
                AU  - Wu, Qin 
                AU  - Shi, Yumeng 
                AU  - Luo, Aishu 
                AU  - Lin, Shiyu 
                AU  - Feng, Xiaoke 
                AU  - Jiang, Jintao 
                AU  - Zhang, Miaojia 
                AU  - Wang, Fang 
                AU  - Tan, Wenfeng 
                TI  - MicroRNA-15a/16/SOX5 axis promotes migration, invasion and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103480
                DO  - 10.18632/aging.103480
                SP  - 14376
                EP  - 14390
                PY  - 
                AB  - Fibroblast-like synoviocytes (FLSs) are key effector cells in the pathogenesis of rheumatoid arthritis (RA) and display a unique aggressive tumor-like phenotype with remarkable hyperplasia, increased cell migration and invasion. How FLSs undergo these changes in RA remains unknown. We previously reported a novel function of transcription factor SOX5 in RA-FLSs that promote cell migration and invasion. In this study, we found that miR-15a/16 directly targets the SOX5 3&#x2019;UTR and suppresses SOX5 expression. Moreover, miR-15a/16 is significantly down-regulated in RA-FLSs, which negatively correlates with SOX5 expression. Transfection with miR-15a/16 mimics in RA-FLSs inhibits cell migration, invasion, IL-1&#x3B2; and TNF&#x3B1; expression. Overexpression SOX5 in RA-FLSs decreases miR-15a/16 expression and rescues miR-15a/16-mediated inhibitory effect. Furthermore, RA patients with the lower baseline serum miR-15a/16 level present poor response of 3 months disease-modifying antirheumatic drugs (DMARDs) therapy. Collectively, this study reveals that miR-15a/16/SOX5 axis functions as a key driver of RA-FLSs invasion, migration and inflammatory response in a mutual negative feedback loop and correlates with DMARDs treatment response in RA.
                ER  -

Click to copy this citation from the text box above or download the citation:

The cross-talk between DDR1 and STAT3 promotes the development of hepatocellular carcinoma

Ye Lin, Haosheng Jin, Xianqiu Wu, Zhixiang Jian, Xiongfeng Zou, Jianfeng Huang, Renguo Guan, Xiangling Wei,

https://doi.org/10.18632/aging.103482 pp 14391—14405

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lin Y, Jin H, Wu X, Jian Z, Zou X, Huang J, Guan R, Wei X, . The cross-talk between DDR1 and STAT3 promotes the development of hepatocellular carcinoma. . 12:14391-14405. https://doi.org/10.18632/aging.103482

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lin, Ye 
                AU  - Jin, Haosheng 
                AU  - Wu, Xianqiu 
                AU  - Jian, Zhixiang 
                AU  - Zou, Xiongfeng 
                AU  - Huang, Jianfeng 
                AU  - Guan, Renguo 
                AU  - Wei, Xiangling 
                TI  - The cross-talk between DDR1 and STAT3 promotes the development of hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103482
                DO  - 10.18632/aging.103482
                SP  - 14391
                EP  - 14405
                PY  - 
                AB  - Objective: To investigate the function of discoidin domain receptor 1 (DDR1) in hepatocellular carcinoma (HCC) and to further clarify the underlying mechanism.
                Results: DDR1 was significantly increased in HCC tissues and cells, which was related to clinical staging and prognosis of HCC. Upregulation of DDR1 promoted EMT and glutamine metabolism in HCC cells, while loss of DDR1 showed the opposite effects. STAT3 bound with the promoter of DDR1, and facilitated the phosphorylation of STAT3. In turn, activation of STAT3 increased the expression of DDR1. Silencing of STAT3 removed the promoting effect of DDR1 on proliferation, migration and invasion of HCC cells. The in vivo tumor growth assay showed that the cross-talk between DDR1 and STAT3 promoted HCC tumorigenesis.
                Conclusions: Our research revealed the positive feedback of DDR1 and STAT3 promoted EMT and glutamine metabolism in HCC, which provided some experimental basis for clinical treatment or prevention of HCC.
                Materials and methods: The mRNA expression of DDR1 was detected by qRT-PCR. CCK8 assay, wound healing assay and transwell assay were used to detect the DDR1/ STAT3 function on proliferation, migration and invasion in HCC cells. Western blot was used to calculate protein level of DDR1, STAT3, epithelial-mesenchymal transition (EMT) related proteins.
                ER  -

Click to copy this citation from the text box above or download the citation:

Osthole resensitizes CD133⁺ hepatocellular carcinoma cells to cisplatin treatment via PTEN/AKT pathway

Junfeng Ye, Di Sun, Ying Yu, Jinhai Yu,

https://doi.org/10.18632/aging.103484 pp 14406—14417

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ye J, Sun D, Yu Y, Yu J, . Osthole resensitizes CD133⁺ hepatocellular carcinoma cells to cisplatin treatment via PTEN/AKT pathway. . 12:14406-14417. https://doi.org/10.18632/aging.103484

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Ye, Junfeng 
 AU - Sun, Di 
 AU - Yu, Ying 
 AU - Yu, Jinhai 
 TI - Osthole resensitizes CD133+ hepatocellular carcinoma cells to cisplatin treatment via PTEN/AKT pathway
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103484
 DO - 10.18632/aging.103484
 SP - 14406
 EP - 14417
 PY - 
 AB - The population of CD133 positive cancer cells has been reported to be responsible for drug resistance of hepatocellular carcinoma (HCC). However, the potential molecular mechanism by which CD133+ HCC cells develop drug resistance is still unclear. In this study, we found that CD133+ HepG2 and Huh7 cells were resistant to cisplatin treatment, compared to the CD133- HepG2 and Huh7 cells. However, treatment with osthole, a natural coumarin isolated from umbelliferae plant monomers, was found to resensitize CD133+ HepG2 and Huh7 cells to cisplatin treatment. In the mechanism research, we found that treatment with osthole increased the expression of PTEN. As a result, osthole inhibited the phosphorylation of AKT and Bad to decrease the amount of free Bcl-2 in CD133+ HepG2 and Huh7 cells. Finally, cisplatin-induced mitochondrial apoptosis was expanded. In conclusion, combination treatment with osthole can resensitize CD133+ HCC cells to cisplatin treatment via the PTEN/AKT pathway.
 ER -

Click to copy this citation from the text box above or download the citation:

miR-5089-5p suppresses castration-resistant prostate cancer resistance to enzalutamide and metastasis via miR-5089-5p/SPINK1/ MAPK/MMP9 signaling

Zhi-Chao Wang, Yan Li, Ke-Liang Wang, Lu Wang, Bo-Sen You, Dan-Feng Zhao, Zhong-Qing Liu, Rui-Zhe Fang, Jia-Qi Wang, Wei Zhang, Jin-Ming Zhang, Wan-Hai Xu,

https://doi.org/10.18632/aging.103485 pp 14418—14433

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang Z, Li Y, Wang K, Wang L, You B, Zhao D, Liu Z, Fang R, Wang J, Zhang W, Zhang J, Xu W, . miR-5089-5p suppresses castration-resistant prostate cancer resistance to enzalutamide and metastasis via miR-5089-5p/SPINK1/ MAPK/MMP9 signaling. . 12:14418-14433. https://doi.org/10.18632/aging.103485

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Zhi-Chao 
                AU  - Li, Yan 
                AU  - Wang, Ke-Liang 
                AU  - Wang, Lu 
                AU  - You, Bo-Sen 
                AU  - Zhao, Dan-Feng 
                AU  - Liu, Zhong-Qing 
                AU  - Fang, Rui-Zhe 
                AU  - Wang, Jia-Qi 
                AU  - Zhang, Wei 
                AU  - Zhang, Jin-Ming 
                AU  - Xu, Wan-Hai 
                TI  - miR-5089-5p suppresses castration-resistant prostate cancer resistance to enzalutamide and metastasis via miR-5089-5p/SPINK1/ MAPK/MMP9 signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103485
                DO  - 10.18632/aging.103485
                SP  - 14418
                EP  - 14433
                PY  - 
                AB  - Whether serine protease inhibitor Kazal type 1 (SPINK1) being associated with enzalutamide (Enz) resistance and metastasis of castration-resistant prostate cancer (CRPC) has not been clear. SPINK1 promoted Enz resistance by upregulating Androgen receptor splicing variant 7 (ARv7), and enhanced the invasion/migration of Enz-resistant cells via ERK/p38/ MMP9 signaling. Furthermore, miR-5089-5p suppressed SPINK1 mRNA through direct binding to its 3&apos;UTR, and reversed its pro-proliferative and pro-metastatic effects. Mice bearing SPINK1-knockdown Enz-resistant PCa tumors showed significantly longer survival compared with those bearing wild-type tumors, while treatment with miR-5089-5p inhibitor abrogated the protective effects of SPINK1 knockdown. Taken together, SPINK1 can be used as a biomarker of resistance to Enz, and the miR-5089-5p/SPINK1/MAPK/MMP9 axis is a suitable therapeutic target against Enz-resistant and metastatic CRPC.Methods: The expression of SPINK1 in Enz-resistant prostate cancer (PCa) cell lines was detected through next-generation sequencing data and metastatic PCa patients. In vivo and in vitro experiments were performed to investigate the role of SPINK1 in Enz-resistance and metastasis.
                ER  -

Click to copy this citation from the text box above or download the citation:

Characterization of aberrant pathways activation and immune microenviroment of BK virus associated nephropathy

Yongguang Liu, Song Zhou, Jianmin Hu, Wentao Xu, Ding Liu, Jun Liao, Guorong Liao, Zefeng Guo, Yuzhu Li, Siqiang Yang, Shichao Li, Hua Chen, Ying Guo, Ming Li, Lipei Fan, Liuyang Li, Anqi Lin, Ming Zhao,

https://doi.org/10.18632/aging.103486 pp 14434—14451

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liu Y, Zhou S, Hu J, Xu W, Liu D, Liao J, Liao G, Guo Z, Li Y, Yang S, Li S, Chen H, Guo Y, et al, . Characterization of aberrant pathways activation and immune microenviroment of BK virus associated nephropathy. . 12:14434-14451. https://doi.org/10.18632/aging.103486

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liu, Yongguang 
                AU  - Zhou, Song 
                AU  - Hu, Jianmin 
                AU  - Xu, Wentao 
                AU  - Liu, Ding 
                AU  - Liao, Jun 
                AU  - Liao, Guorong 
                AU  - Guo, Zefeng 
                AU  - Li, Yuzhu 
                AU  - Yang, Siqiang 
                AU  - Li, Shichao 
                AU  - Chen, Hua 
                AU  - Guo, Ying 
                AU  - Li, Ming 
                AU  - Fan, Lipei 
                AU  - Li, Liuyang 
                AU  - Lin, Anqi 
                AU  - Zhao, Ming 
                TI  - Characterization of aberrant pathways activation and immune microenviroment of BK virus associated nephropathy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103486
                DO  - 10.18632/aging.103486
                SP  - 14434
                EP  - 14451
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Liu, Yongguang 
                AU  - Zhou, Song 
                AU  - Hu, Jianmin 
                AU  - Xu, Wentao 
                AU  - Liu, Ding 
                AU  - Liao, Jun 
                AU  - Liao, Guorong 
                AU  - Guo, Zefeng 
                AU  - Li, Yuzhu 
                AU  - Yang, Siqiang 
                AU  - Li, Shichao 
                AU  - Chen, Hua 
                AU  - Guo, Ying 
                AU  - Li, Ming 
                AU  - Fan, Lipei 
                AU  - Li, Liuyang 
                AU  - Lin, Anqi 
                AU  - Zhao, Ming 
                TI  - Characterization of aberrant pathways activation and immune microenviroment of BK virus associated nephropathy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103486
                DO  - 10.18632/aging.103486
                SP  - 14434
                EP  - 14451
                PY  - 
                AB  - In the context of transplantation with the use of immunosuppressive drugs, BK virus infection has become the main cause of BK virus nephropathy(BKVN) in renal transplant recipients(KTRs). More importantly, BKVN may cause further allograft dysfunction and loss. However, the role of the immune microenvironment in the pathogenesis of BKVN remains unknown. Therefore, we collected microarray data of KTRs to elucidate the immune characteristics of BKVN. Via the CIBERSORT, we found that BKVN had relatively more activated memory CD4 T cells. Immunostaining showed that CD4+ and CD8+cells were significantly different between BKVN and stable allografts(STAs). In addition, the expression of immune-related genes(antigen presentation, cytotoxicity, and inflammation) was significantly higher in BKVN than in STAs. The results of gene set enrichment analysis(GSEA) and single-sample GSEA(ssGSEA) indicated that immune cell-,cytokine-,chemokine-, and inflammation-related pathways were significantly activated in BKVN, while metabolism- and renal development-related pathways were significantly downregulated in BKVN. In addition, the immune microenvironments of the peripheral blood in patients with BK viremia(BKV) or transplant kidney biopsy(TKB) with BKVN may be different. Overall, the immune microenvironment may play important roles in the occurrence and development of BKVN and provide a theoretical basis for preventing the occurrence of BKVN and finding novel treatments.
                ER  -

Click to copy this citation from the text box above or download the citation:

Long noncoding RNA LINC01559 promotes pancreatic cancer progression by acting as a competing endogenous RNA of miR-1343-3p to upregulate RAF1 expression

Xiao Chen, Jie Wang, Fei Xie, Tinggang Mou, Pingyong Zhong, Hao Hua, Pan Liu, Qin Yang,

https://doi.org/10.18632/aging.103487 pp 14452—14466

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen X, Wang J, Xie F, Mou T, Zhong P, Hua H, Liu P, Yang Q, . Long noncoding RNA LINC01559 promotes pancreatic cancer progression by acting as a competing endogenous RNA of miR-1343-3p to upregulate RAF1 expression. . 12:14452-14466. https://doi.org/10.18632/aging.103487

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Xiao 
                AU  - Wang, Jie 
                AU  - Xie, Fei 
                AU  - Mou, Tinggang 
                AU  - Zhong, Pingyong 
                AU  - Hua, Hao 
                AU  - Liu, Pan 
                AU  - Yang, Qin 
                TI  - Long noncoding RNA LINC01559 promotes pancreatic cancer progression by acting as a competing endogenous RNA of miR-1343-3p to upregulate RAF1 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103487
                DO  - 10.18632/aging.103487
                SP  - 14452
                EP  - 14466
                PY  - 
                AB  - Background: An increasing number of studies have shown that lncRNAs are involved in the biological processes of pancreatic cancer (PC). Hence, we investigated the role of a novel noncoding RNA, LINC01559, involved in PC progression.Results: LINC01559 and RAF1 were highly expressed in PC, while miR-1343-3p had low expression. High expression of LINC01559 was significantly associated with large tumors, lymph node metastasis, and poor prognosis. Functional experiment results revealed that silencing of LINC01559 significantly suppressed PC cell proliferation and metastasis. Meanwhile, LINC01559 could act as a ceRNA to competitively sponge miR-1343-3p to up-regulate RAF1 and activate its downstream ERK pathwayConclusions: LINC01559 functions as an oncogene in PC progression through acting as a ceRNA of miR-1343-3p. Hence, LINC01559 is a potential diagnostic and therapeutic target.Methods: RT-qPCR was performed to determine the expression of LINC01559 and miR-1343-3p in PC. Individual patient data were collected to investigate the correlation between clinicopathological features and LINC01559 expression. Subsequently, the expression of LINC01559, miR-1343-3p, and RAF1 was altered using transfection of vectors or inhibitors. Gain- and loss-of-function assays and mechanistic assays were applied to verify the effects of LINC01559, miR-1343-3p, and RAF1 on PC cell proliferation and metastasis in vivo and in vitro.
                ER  -

Click to copy this citation from the text box above or download the citation:

The regulatory role of miR-107 in Coxsackie B3 virus replication

Min Yao, Chi Xu, Hongxing Shen, Tingjun Liu, Xiuping Wang, Chen Shao, Shihe Shao,

https://doi.org/10.18632/aging.103488 pp 14467—14479

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Yao M, Xu C, Shen H, Liu T, Wang X, Shao C, Shao S, . The regulatory role of miR-107 in Coxsackie B3 virus replication. . 12:14467-14479. https://doi.org/10.18632/aging.103488

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Yao, Min 
                AU  - Xu, Chi 
                AU  - Shen, Hongxing 
                AU  - Liu, Tingjun 
                AU  - Wang, Xiuping 
                AU  - Shao, Chen 
                AU  - Shao, Shihe 
                TI  - The regulatory role of miR-107 in Coxsackie B3 virus replication
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103488
                DO  - 10.18632/aging.103488
                SP  - 14467
                EP  - 14479
                PY  - 
                AB  - Coxsackie B3 virus (CVB3) is a member of small RNA viruses that belongs to the genus Enterovirus of the family Picornaviridae and CVB3 is the main pathogen of acute and chronic viral myocarditis. In this study RT-qPCR was used to determine the expression of miR-107 in CVB3-infected and uninfected HeLa cells. The experimental results show that the level of miR-107 began to rise at 4 h after the infection, and significantly boosted at 6 h. Based on the results of this experiment, we consider that miR-107 expression is related to CVB3 infection. In order to further clarify the effect of miR-107 in the process of CVB3 infection, we studied the effect of miR-107 upstream and downstream target genes on CVB3 replication. Levels of the target RNAs were detected by RT-qPCR after CVB3 infection, and the expression of CVB3 capsid protein VP1 by western blot analysis. Then the virus in the supernatant was quantitated via a viral plaque assay, reflecting the release of the virus. The experimental results showed that miRNA-107 expression is associated with CVB3 replication and proliferation, while KLF4 and BACE1 as the downstream of miR-107 weakened CVB3 replication. Overexpressions of KLF4 and BACE1 negatively regulated CVB3 replication, this effect on CVB3 was completely opposite to that of miR-107. Further experiments revealed that the upstream lncRNA004787, a new lncRNA that had not been reported, was located on chromosome 5, strand - from 37073250 to 37070908 (genome assembly: hg19). We sequenced and studied lncRNA004787 and found that it partially inhibited CVB3 replication. This prompted us to speculate that lncRNA004787 probably impacted the replication by other means. In conclusion, miR-107 interfered with CVB3 replication and release.
                ER  -

Click to copy this citation from the text box above or download the citation:

MiR-135a inhibits non-small cell lung cancer progression by suppressing RAB1B expression and the RAS pathway

Ye Tian, Lei Zhang, Qian Yu, Zelong Wang, Xueying Yang,

https://doi.org/10.18632/aging.103494 pp 14480—14489

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Tian Y, Zhang L, Yu Q, Wang Z, Yang X, . MiR-135a inhibits non-small cell lung cancer progression by suppressing RAB1B expression and the RAS pathway. . 12:14480-14489. https://doi.org/10.18632/aging.103494

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Tian, Ye 
                AU  - Zhang, Lei 
                AU  - Yu, Qian 
                AU  - Wang, Zelong 
                AU  - Yang, Xueying 
                TI  - MiR-135a inhibits non-small cell lung cancer progression by suppressing RAB1B expression and the RAS pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103494
                DO  - 10.18632/aging.103494
                SP  - 14480
                EP  - 14489
                PY  - 
                AB  - Lung cancer is the most common tumor in China and worldwide. Despite advances in diagnosis and therapy, it still represents the most lethal malignancy in industrialized countries. The study of regulatory noncoding RNAs has deepened our understanding of cancer on the molecular and clinical level. In this article, it showed that miR-135a was aberrantly downregulated in non-small cell lung cancer (NSCLC) cells in comparison with normal bronchial epithelial cells, and the expression of miR-135a inhibited proliferation, invasion and metastasis of NSCLC cells in vitro. Moreover, it was demonstrated that miR-135a inhibited the expression of multiple components (including RAS, Raf1, Rac1 and RhoA) of the RAS pathway via RAB1B, which was a novel target of miR-135a. The expression of miR-135a and RAB1B could effectively predict the clinical outcomes of NSCLC. In summary, miR-135a might function as a suppressor of NSCLC cells, and thus could be used as a potential therapeutic target.
                ER  -

Click to copy this citation from the text box above or download the citation:

RNA-seq analysis of the key long noncoding RNAs and mRNAs related to cognitive impairment after cardiac arrest and cardiopulmonary resuscitation

Chan Chen, Changliang Liu, Zhendong Niu, Ming Li, Yuhan Zhang, Rui Gao, Hai Chen, Qiao Wang, Shu Zhang, Ronghua Zhou, Lu Gan, Zheng Zhang, Tao Zhu, Hai Yu, Jin Liu,

https://doi.org/10.18632/aging.103495 pp 14490—14505

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen C, Liu C, Niu Z, Li M, Zhang Y, Gao R, Chen H, Wang Q, Zhang S, Zhou R, Gan L, Zhang Z, Zhu T, et al, . RNA-seq analysis of the key long noncoding RNAs and mRNAs related to cognitive impairment after cardiac arrest and cardiopulmonary resuscitation. . 12:14490-14505. https://doi.org/10.18632/aging.103495

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Chan 
                AU  - Liu, Changliang 
                AU  - Niu, Zhendong 
                AU  - Li, Ming 
                AU  - Zhang, Yuhan 
                AU  - Gao, Rui 
                AU  - Chen, Hai 
                AU  - Wang, Qiao 
                AU  - Zhang, Shu 
                AU  - Zhou, Ronghua 
                AU  - Gan, Lu 
                AU  - Zhang, Zheng 
                AU  - Zhu, Tao 
                AU  - Yu, Hai 
                AU  - Liu, Jin 
                TI  - RNA-seq analysis of the key long noncoding RNAs and mRNAs related to cognitive impairment after cardiac arrest and cardiopulmonary resuscitation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103495
                DO  - 10.18632/aging.103495
                SP  - 14490
                EP  - 14505
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Chen, Chan 
                AU  - Liu, Changliang 
                AU  - Niu, Zhendong 
                AU  - Li, Ming 
                AU  - Zhang, Yuhan 
                AU  - Gao, Rui 
                AU  - Chen, Hai 
                AU  - Wang, Qiao 
                AU  - Zhang, Shu 
                AU  - Zhou, Ronghua 
                AU  - Gan, Lu 
                AU  - Zhang, Zheng 
                AU  - Zhu, Tao 
                AU  - Yu, Hai 
                AU  - Liu, Jin 
                TI  - RNA-seq analysis of the key long noncoding RNAs and mRNAs related to cognitive impairment after cardiac arrest and cardiopulmonary resuscitation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103495
                DO  - 10.18632/aging.103495
                SP  - 14490
                EP  - 14505
                PY  - 
                AB  - Cardiac arrest (CA) is the leading cause of death around the world. Survivors after CA and cardiopulmonary resuscitation (CPR) develop moderate to severe cognitive impairment up to 60% at 3 months. Accumulating evidence demonstrated that long non-coding RNAs (lncRNAs) played a pivotal role in ischemic brain injury. This study aimed to identify potential key lncRNAs associated with early cognitive deficits after CA/CPR. LncRNA and mRNA expression profiles of the hippocampus in CA/CPR or sham group were analyzed via high-throughput RNA sequencing, which exhibited 1920 lncRNAs and 1162 mRNAs were differentially expressed. These differentially expressed genes were confirmed to be primarily associated with inflammatory or apoptotic signaling pathways through GO and KEGG pathway enrichment analysis and coding-noncoding co-expression network analysis. Among which, five key pairs of lncRNA-mRNA were further analyzed by qRT-PCR and western blot. We found that the lncRNANONMMUT113601.1 and mRNA Shc1, an inflammation and apoptosis-associated gene, exhibited the most significant changes in hippocampus of CA/CPR mice. Furthermore, we found that the correlations between this lncRNA and mRNA mainly happened in neurons of hippocampus by in situ hybridization. These results suggested that the critical pairs of lncRNA-mRNA may act as essential regulators in early cognitive deficits after resuscitation.
                ER  -

Click to copy this citation from the text box above or download the citation:

Identification of lncRNA biomarkers for lung cancer through integrative cross-platform data analyses

Tianying Zhao, Vedbar Singh Khadka, Youping Deng,

https://doi.org/10.18632/aging.103496 pp 14506—14527

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhao T, Khadka VS, Deng Y, . Identification of lncRNA biomarkers for lung cancer through integrative cross-platform data analyses. . 12:14506-14527. https://doi.org/10.18632/aging.103496

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhao, Tianying 
                AU  - Khadka, Vedbar Singh 
                AU  - Deng, Youping 
                TI  - Identification of lncRNA biomarkers for lung cancer through integrative cross-platform data analyses
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103496
                DO  - 10.18632/aging.103496
                SP  - 14506
                EP  - 14527
                PY  - 
                AB  - This study was designed to identify lncRNA biomarker candidates using lung cancer data from RNA-Seq and microarray platforms separately.Lung cancer datasets were obtained from the Gene Expression Omnibus (GEO, n = 287) and The Cancer Genome Atlas (TCGA, n = 216) repositories, only common lncRNAs were used. Differentially expressed (DE) lncRNAs in tumors with respect to normal were selected from the Affymetrix and TCGA datasets. A training model consisting of the top 20 DE Affymetrix lncRNAs was used for validation in the TCGA and Agilent datasets. A second similar training model was generated using the TCGA dataset.First, a model using the top 20 DE lncRNAs from Affymetrix for training and validated using TCGA and Agilent, achieved high prediction accuracy for both training (98.5% AUC for Affymetrix) and validation (99.2% AUC for TCGA and 92.8% AUC for Agilent). A similar model using the top 20 DE lncRNAs from TCGA for training and validated using Affymetrix and Agilent, also achieved high prediction accuracy for both training (97.7% AUC for TCGA) and validation (96.5% AUC for Affymetrix and 80.9% AUC for Agilent). Eight lncRNAs were found to be overlapped from these two lists.
                ER  -

Click to copy this citation from the text box above or download the citation:

Plasma sex hormone-binding globulin predicts neurodegeneration and clinical progression in prodromal Alzheimer's disease

Wei Xu, Bing-Jie Su, Xue-Ning Shen, Yan-Lin Bi, Chen-Chen Tan, Jie-Qiong Li, Xi-Peng Cao, Qiang Dong, Lan Tan, Alzheimer’s Disease Neuroimaging Initiative, Jin-Tai Yu,

https://doi.org/10.18632/aging.103497 pp 14528—14541

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu W, Su B, Shen X, Bi Y, Tan C, Li J, Cao X, Dong Q, Tan L, , Yu J, . Plasma sex hormone-binding globulin predicts neurodegeneration and clinical progression in prodromal Alzheimer's disease. . 12:14528-14541. https://doi.org/10.18632/aging.103497

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xu, Wei 
                AU  - Su, Bing-Jie 
                AU  - Shen, Xue-Ning 
                AU  - Bi, Yan-Lin 
                AU  - Tan, Chen-Chen 
                AU  - Li, Jie-Qiong 
                AU  - Cao, Xi-Peng 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - ,  
                AU  - Yu, Jin-Tai 
                TI  - Plasma sex hormone-binding globulin predicts neurodegeneration and clinical progression in prodromal Alzheimer's disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103497
                DO  - 10.18632/aging.103497
                SP  - 14528
                EP  - 14541
                PY  - 
                AB  - It was unclear whether sex hormone-binding globulin (SHBG) was a circulating biomarker of Alzheimer&#x2019;s disease (AD). We tested the cross-sectional relationships between plasma SHBG and cerebrospinal fluid (CSF) AD biomarkers in 707 non-demented adults. Next, the influences of plasma SHBG on dynamic changes of CSF A&#x3B2;42, hippocampus volume, brain metabolism, and cognition were explored in 448 non-demented adults from the Alzheimer&#x2019;s disease Neuroimaging Initiative (ADNI). Finally, the predictive and diagnostic values of plasma SHBG in AD were explored. A positive correlation was found between SHBG levels in plasma and CSF. Individuals with higher plasma SHBG levels had lower CSF A&#x3B2;42 (p &lt; 0.005), after adjusting for age, gender, education, APOE4 allele, and cognitive scores. Though no significant difference of plasma SHBG was observed between mild AD dementia and healthy normal, plasma SHBG could contribute to accelerated rates of CSF A&#x3B2;42 decrease (p &lt; 0.0005), decline in brain metabolism (p &lt; 0.05), and hippocampus atrophy (p &lt; 0.01), cognitive decline (p &lt; 0.01), as well as higher risk of AD dementia (p &lt; 0.05). These findings indicated plasma SHBG could be a prodromal biomarker to predict disease progression in AD.
                ER  -

Click to copy this citation from the text box above or download the citation:

Higher expression of cell division cycle-associated protein 5 predicts poorer survival outcomes in hepatocellular carcinoma

Shengzhong Hou, Xing Chen, Mao Li, Xing Huang, Haotian Liao, Bole Tian,

https://doi.org/10.18632/aging.103501 pp 14542—14555

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Hou S, Chen X, Li M, Huang X, Liao H, Tian B, . Higher expression of cell division cycle-associated protein 5 predicts poorer survival outcomes in hepatocellular carcinoma. . 12:14542-14555. https://doi.org/10.18632/aging.103501

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Hou, Shengzhong 
                AU  - Chen, Xing 
                AU  - Li, Mao 
                AU  - Huang, Xing 
                AU  - Liao, Haotian 
                AU  - Tian, Bole 
                TI  - Higher expression of cell division cycle-associated protein 5 predicts poorer survival outcomes in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103501
                DO  - 10.18632/aging.103501
                SP  - 14542
                EP  - 14555
                PY  - 
                AB  - The upregulation of cell division cycle associated protein 5 (CDCA5) has been observed in various cancer types. However, the prognostic value of CDCA5 and its underlying mechanism contributing to tumorigenesis in hepatocellular carcinoma (HCC) remain poorly understood. We used tissue microarray (TMA) to evaluate the prognosis of 304 HCC samples based on their CDCA5 expression, and analyzed the genomic features correlated with CDCA5 by using dataset from The Cancer Genome Atlas (TCGA). Compared with adjacent normal tissues, increased expression of CDCA5 was found in HCC tissues. Moreover, higher expression of CDCA5 was associated with inferior OS and DFS outcomes in HCC patients. The enrichment plots showed that the gene signatures in cell cycle, DNA replication and p53 pathways were enriched in patients with higher CDCA5 expression. Meanwhile, statistically higher mutations burdens in TP53 could also be observed in CDCA5-high patients. Integrative analysis based on miRNAseq and methylation data demonstrated a potential association between CDCA5 expression and epigenetic changes. In conclusion, our study provided the evidence of CDCA5 as an oncogenic promoter in HCC and the potential function of CDCA5 in affecting tumor microenvironment.
                ER  -

Click to copy this citation from the text box above or download the citation:

TP53 somatic mutations are associated with poor survival in non-small cell lung cancer patients who undergo immunotherapy

Liqin Zhao, Xiaofei Qu, Zhenhua Wu, Yuehua Li, Xiaowei Zhang, WeiJian Guo,

https://doi.org/10.18632/aging.103502 pp 14556—14568

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhao L, Qu X, Wu Z, Li Y, Zhang X, Guo W, . TP53 somatic mutations are associated with poor survival in non-small cell lung cancer patients who undergo immunotherapy. . 12:14556-14568. https://doi.org/10.18632/aging.103502

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Zhao, Liqin 
 AU - Qu, Xiaofei 
 AU - Wu, Zhenhua 
 AU - Li, Yuehua 
 AU - Zhang, Xiaowei 
 AU - Guo, WeiJian 
 TI - TP53 somatic mutations are associated with poor survival in non-small cell lung cancer patients who undergo immunotherapy
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103502
 DO - 10.18632/aging.103502
 SP - 14556
 EP - 14568
 PY - 
 AB - In this study, we investigated the association between TP53 somatic mutations and immunotherapeutic outcomes in non-small cell lung cancer (NSCLC) patients. Kaplan-Meier survival curve analysis of the MSK-IMPACT cohort of 350 NSCLC patients shows that overall survival (OS) is significantly lower for patients with truncating TP53 mutations than those with wild-type TP53 (OS: 9 months vs. 14 months; P=0.019). Multivariate analysis shows that truncating TP53 mutations are an independent predictor of immunotherapeutic outcomes. Moreover, among NSCLC patients with lower tumor mutation burden (TMB), those with TP53 truncating mutations showed significantly lower OS than those with wild-type TP53 [hazard ratio (HR) = 1.40, confidence interval (CI) = 1.13-1.73; P = 0.002]. TP53 mutations correlate with higher infiltration of CD8+ T cells, neutrophils and dendritic cells in lung adenocarcinoma tissues. A prognostic model with TP53 mutational status shows better survival prediction than the model without TP53 mutational status 1-year [area under curve (AUC): 64.9% vs. 60.2%; P = 0.052] and 2-years (AUC: 70.9% vs. 66.1%; P = 0.098) post-immunotherapy. These findings demonstrate that truncating TP53 mutations correlate with poor immunotherapy outcomes in NSCLC patients with low TMB. TP53 mutation status also improves the prognostic prediction in NSCLC patients that underwent immunotherapy.
 ER -

Click to copy this citation from the text box above or download the citation:

High serum uric acid is associated with increased arterial stiffness in hypertension

Li-Na An, Ning Rong, Min Ning, Liu-Liu Feng, Zhen-Han Chen, Wei-Qing Liu, Xiao-Chun Ouyang, Fan-Rong Diao, Zhi-Gang Han, Jiang Hong,

https://doi.org/10.18632/aging.103506 pp 14569—14581

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

An L, Rong N, Ning M, Feng L, Chen Z, Liu W, Ouyang X, Diao F, Han Z, Hong J, . High serum uric acid is associated with increased arterial stiffness in hypertension. . 12:14569-14581. https://doi.org/10.18632/aging.103506

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - An, Li-Na 
                AU  - Rong, Ning 
                AU  - Ning, Min 
                AU  - Feng, Liu-Liu 
                AU  - Chen, Zhen-Han 
                AU  - Liu, Wei-Qing 
                AU  - Ouyang, Xiao-Chun 
                AU  - Diao, Fan-Rong 
                AU  - Han, Zhi-Gang 
                AU  - Hong, Jiang 
                TI  - High serum uric acid is associated with increased arterial stiffness in hypertension
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103506
                DO  - 10.18632/aging.103506
                SP  - 14569
                EP  - 14581
                PY  - 
                AB  - Serum uric acid level has been found to be associated with cerebrovascular diseases. However, whether serum uric acid level is a risk factor for arterial stiffness in the hypertension population is unclear. This study was designed to determine the relationship between serum uric acid level and arterial stiffness in the hypertension population. A total of 10450 participants were evaluated for the risk of arterial stiffness. Brachial-ankle pulse wave velocity (baPWV) was assessed, and high baPWV was determined as the highest quartile of baPWV values in a sex-specific manner. We evaluated the association between serum uric acid level and baPWV through multivariate-adjusted linear and logistic regression analyses. There was a significant difference on high baPWV between patients with quartiles of serum uric acid level in females and males (p&lt;0.01), respectively. The odds ratios (95% CI) of the highest baPWV quartile across the sex-specific serum uric acid level were 1.0, 1.71 (1.35, 2.17), 1.75 (1.38, 2.23), and 1.95 (1.51, 2.51) in female, and 1.0, 1.33 (1.09, 1.64), 1.36 (1.11, 1.67), and 1.67 (1.36, 2.04) in male after adjusting for potential confounders. In conclusion, serum uric acid level could be considered as an important risk factor for arterial stiffness in Chinese hypertension population.
                ER  -

Click to copy this citation from the text box above or download the citation:

Construction of a prognosis-predicting model based on autophagy-related genes for hepatocellular carcinoma (HCC) patients

Yayun Zhu, Ru Wang, Wanbin Chen, Qiuyu Chen, Jian Zhou,

https://doi.org/10.18632/aging.103507 pp 14582—14592

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhu Y, Wang R, Chen W, Chen Q, Zhou J, . Construction of a prognosis-predicting model based on autophagy-related genes for hepatocellular carcinoma (HCC) patients. . 12:14582-14592. https://doi.org/10.18632/aging.103507

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhu, Yayun 
                AU  - Wang, Ru 
                AU  - Chen, Wanbin 
                AU  - Chen, Qiuyu 
                AU  - Zhou, Jian 
                TI  - Construction of a prognosis-predicting model based on autophagy-related genes for hepatocellular carcinoma (HCC) patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103507
                DO  - 10.18632/aging.103507
                SP  - 14582
                EP  - 14592
                PY  - 
                AB  - Background: Autophagy, a highly conserved cellular catabolic process by which the eukaryotic cells deliver autophagosomes engulfing cellular proteins and organelles to lysosomes for degradation, is critical for maintaining cellular homeostasis in response to various signals and nutrient stresses. The dysregulation of autophagy has been noted in the pathogenesis of cancers. Our study aims to investigate the prognosis-predicting value of autophagy-related genes (ARG) in hepatocellular carcinoma (HCC).Results: The signature was constructed based on eight ARGs, which stratified HCC patients into high- and low-risk groups in terms of overall survival (OS) (Hazard Ratio, HR=4.641, 95% Confidential Interval, CI, 3.365-5.917, P=0.000). The ARG signature is an independent prognostic indicator for HCC patients (HR = 1.286, 95% CI, 1.194-1.385; P &lt; 0.001). The area under the receiver operating characteristic (ROC) curve (AUC) for 5-year survival is 0.765.Conclusion: This study provides a potential prognostic signature for predicting the prognosis of HCC patients and molecular insights into the significance of autophagy in HCC.Methods: Sixty-two differentially expressed ARGs and the clinical characteristics and basic information of the 369 enrolled HCC patients were retrieved from The Cancer Genome Atlas (TCGA) database. the Cox proportional hazard regression analysis was adopted to identify survival-related ARGs, based on which a prognosis predicting signature was constructed.
                ER  -

Click to copy this citation from the text box above or download the citation:

Radiomics-based prediction of survival in patients with head and neck squamous cell carcinoma based on pre- and post-treatment ¹⁸F-PET/CT

Zheran Liu, Yuan Cao, Wei Diao, Yue Cheng, Zhiyun Jia, Xingchen Peng,

https://doi.org/10.18632/aging.103508 pp 14593—14619

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liu Z, Cao Y, Diao W, Cheng Y, Jia Z, Peng X, . Radiomics-based prediction of survival in patients with head and neck squamous cell carcinoma based on pre- and post-treatment ¹⁸F-PET/CT. . 12:14593-14619. https://doi.org/10.18632/aging.103508

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Liu, Zheran 
 AU - Cao, Yuan 
 AU - Diao, Wei 
 AU - Cheng, Yue 
 AU - Jia, Zhiyun 
 AU - Peng, Xingchen 
 TI - Radiomics-based prediction of survival in patients with head and neck squamous cell carcinoma based on pre- and post-treatment 18F-PET/CT
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103508
 DO - 10.18632/aging.103508
 SP - 14593
 EP - 14619
 PY - 
 AB - Background: 18-fluorodeoxyglucose positron emission tomography/computed tomography (18F-PET/CT) has been widely applied for the imaging of head and neck squamous cell carcinoma (HNSCC). This study examined whether pre- and post-treatment 18F-PET/CT features can help predict the survival of HNSCC patients.Results: Three radiomics features were identified as prognostic factors. Radiomics score calculated from these features significantly predicted overall survival (OS) and disease-free disease (DFS). The clinicopathological characteristics combined with pre- or post-treatment nomograms showed better ROC curves and decision curves than the nomogram based only on clinicopathological characteristics.Conclusions: Combining clinicopathological characteristics with radiomics features of pre-treatment PET/CT or post-treatment PET/CT assessment of primary tumor sites as positive or negative may substantially improve prediction of OS and DFS of HNSCC patients.Methods: 171 patients who received pre-treatment 18F-PET/CT scans and 154 patients who received post-treatment 18F-PET/CT scans with HNSCC in the Cancer Imaging Achieve (TCIA) were included. Nomograms that combined clinicopathological features with either pre-treatment PET/CT radiomics features or post-treatment assessment of primary tumor sites were constructed using data from 154 HNSCC patients. Receiver operating characteristic (ROC) curves and decision curves were used to compare the predictions of these models with those of a model incorporating only clinicopathological features.
 ER -

Click to copy this citation from the text box above or download the citation:

Circadian clock is associated with tumor microenvironment in kidney renal clear cell carcinoma

Liangcheng Zhou, Zhili Luo, Zuwei li, Qinying Huang,

https://doi.org/10.18632/aging.103509 pp 14620—14632

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhou L, Luo Z, li Z, Huang Q, . Circadian clock is associated with tumor microenvironment in kidney renal clear cell carcinoma. . 12:14620-14632. https://doi.org/10.18632/aging.103509

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhou, Liangcheng 
                AU  - Luo, Zhili 
                AU  - li, Zuwei 
                AU  - Huang, Qinying 
                TI  - Circadian clock is associated with tumor microenvironment in kidney renal clear cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103509
                DO  - 10.18632/aging.103509
                SP  - 14620
                EP  - 14632
                PY  - 
                AB  - Background: Kidney renal clear cell carcinoma (KIRC) is one of the most prevalent malignancies with high incidence and mortality. The circadian clock, which is also involved in the regulation of the immune system and tumor microenvironment, is an internal timing system that allows organisms to adjust biological processes and behaviors according to geophysical time.Result: A wide range of circadian clock genes are epigenetically altered in KIRC, and associated with the overall survival and disease-free survival of patients. SNV analysis revealed missense mutation and splice site to be the most common variant types of circadian clock genes in KIRC. Several circadian clock genes were involved in the regulation of some cancer-related hallmark pathways, including apoptosis and cell cycle pathway. Further, immune infiltrates analysis not only revealed that the expression of circadian clock genes is associated with immune cell infiltrates, but also that somatic copy-number alteration of circadian clock genes could inhibit the immune infiltrates. Moreover, enrichment analysis implied that the circadian clock genes could regulate transcription factor activity and circadian rhythm in KIRC.Conclusion: Our results demonstrate the potential of chrono-immunotherapy as a candidate option for the management of KIRC.Method: Multi-omics analysis was performed to comprehensively determine the roles of core circadian clock genes in KIRC.
                ER  -

Click to copy this citation from the text box above or download the citation:

ASNEO: Identification of personalized alternative splicing based neoantigens with RNA-seq

Zhanbing Zhang, Chi Zhou, Lihua Tang, Yukang Gong, Zhiting Wei, Gongchen Zhang, Feng Wang, Qi Liu, Jing Yu,

https://doi.org/10.18632/aging.103516 pp 14633—14648

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhang Z, Zhou C, Tang L, Gong Y, Wei Z, Zhang G, Wang F, Liu Q, Yu J, . ASNEO: Identification of personalized alternative splicing based neoantigens with RNA-seq. . 12:14633-14648. https://doi.org/10.18632/aging.103516

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Zhang, Zhanbing 
 AU - Zhou, Chi 
 AU - Tang, Lihua 
 AU - Gong, Yukang 
 AU - Wei, Zhiting 
 AU - Zhang, Gongchen 
 AU - Wang, Feng 
 AU - Liu, Qi 
 AU - Yu, Jing 
 TI - ASNEO: Identification of personalized alternative splicing based neoantigens with RNA-seq
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103516
 DO - 10.18632/aging.103516
 SP - 14633
 EP - 14648
 PY - 
 AB - Cancer neoantigens have shown great potential in immunotherapy, while current software focuses on identifying neoantigens which are derived from SNVs, indels or gene fusions. Alternative splicing widely occurs in tumor samples and it has been proven to contribute to the generation of candidate neoantigens. Here we present ASNEO, which is an integrated computational pipeline for the identification of personalized Alternative Splicing based NEOantigens with RNA-seq. Our analyses showed that ASNEO could identify neopeptides which are presented by MHC I complex through mass spectrometry data validation. When ASNEO was applied to two immunotherapy-treated cohorts, we found that alternative splicing based neopeptides generally have a higher immune score than that of somatic neopeptides and alternative splicing based neopeptides could be a marker to predict patient survival pattern. Our identification of alternative splicing derived neopeptides would contribute to a more complete understanding of the tumor immune landscape. Prediction of patient-specific alternative splicing neopeptides has the potential to contribute to the development of personalized cancer vaccines.
 ER -

Click to copy this citation from the text box above or download the citation:

Identifying CpG methylation signature as a promising biomarker for recurrence and immunotherapy in non–small-cell lung carcinoma

Ruihan Luo, Jing Song, Xiao Xiao, Zhengbo Xie, Zhiyuan Zhao, Wanfeng Zhang, Shiqi Miao, Yongyao Tang, Longke Ran,

https://doi.org/10.18632/aging.103517 pp 14649—14676

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Luo R, Song J, Xiao X, Xie Z, Zhao Z, Zhang W, Miao S, Tang Y, Ran L, . Identifying CpG methylation signature as a promising biomarker for recurrence and immunotherapy in non–small-cell lung carcinoma. . 12:14649-14676. https://doi.org/10.18632/aging.103517

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Luo, Ruihan 
                AU  - Song, Jing 
                AU  - Xiao, Xiao 
                AU  - Xie, Zhengbo 
                AU  - Zhao, Zhiyuan 
                AU  - Zhang, Wanfeng 
                AU  - Miao, Shiqi 
                AU  - Tang, Yongyao 
                AU  - Ran, Longke 
                TI  - Identifying CpG methylation signature as a promising biomarker for recurrence and immunotherapy in non–small-cell lung carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103517
                DO  - 10.18632/aging.103517
                SP  - 14649
                EP  - 14676
                PY  - 
                AB  - Epigenetic alterations are crucial to oncogenesis and regulation of gene expression in non&#x2013;small-cell lung carcinoma (NSCLC). DNA methylation (DNAm) biomarkers may provide molecular-level prediction of relapse risk in cancer. Identification of optimal treatment is warranted for improving clinical management of NSCLC patients. Using machine learning algorithm we identified 4 recurrence predictive CpG methylation markers (cg00253681/ART4, cg00111503/KCNK9, cg02715629/FAM83A, cg03282991/C6orf10) and constructed a risk score model that potently predicted recurrence-free survival and prognosis for patients with NSCLC (P = 0.0002). Integrating genomic, transcriptomic, proteomic and clinical data, the DNAm-based risk score was observed to significantly associate with clinical stage, cell proliferation markers, somatic alterations, tumor mutation burden (TMB) as well as DNA damage response (DDR) genes, and potentially predict the efficacy of immunotherapy. In general, our identified DNAm signature shows a significant correlation to TMB and DDR pathways, and serves as an effective biomarker for predicting NSCLC recurrence and response to immunotherapy. These findings demonstrate the utility of 4-DNAm-marker panel in the prognosis, treatment decision-making and evaluation of therapeutic responses for NSCLC.
                ER  -

Click to copy this citation from the text box above or download the citation:

Expression and prognosis analysis of DNMT family in acute myeloid leukemia

Ting-Juan Zhang, Liu-Chao Zhang, Zi-Jun Xu, Jing-Dong Zhou,

https://doi.org/10.18632/aging.103520 pp 14677—14690

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhang T, Zhang L, Xu Z, Zhou J, . Expression and prognosis analysis of DNMT family in acute myeloid leukemia. . 12:14677-14690. https://doi.org/10.18632/aging.103520

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Zhang, Ting-Juan 
 AU - Zhang, Liu-Chao 
 AU - Xu, Zi-Jun 
 AU - Zhou, Jing-Dong 
 TI - Expression and prognosis analysis of DNMT family in acute myeloid leukemia
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103520
 DO - 10.18632/aging.103520
 SP - 14677
 EP - 14690
 PY - 
 AB - DNA methyltransferases (DNMTs) by regulating DNA methylation play crucial roles in the progression of hematologic malignancies, especially for acute myeloid leukemia (AML). Accumulating investigations have identified the high incidence of DNMT3A mutation in AML, and it is correlated with poor prognosis. Although a few studies have shown the expression of DNMTs and their clinical significance in AML, the results remain to be discussed. Herein, we systemically analyzed the DNMTs expression and their relationship with clinic-pathological features and prognosis in AML patients. DNMTs expression especially for DNMT3A/3B was closely associated with AML among various human cancers. DNMT3A expression was increased in AML patients, whereas DNMT3B expression was decreased. Significant associations between DNMT3A/B expression and clinic-pathological features/gene mutations were observed. Kaplan-Meier analysis showed that DNMT3A expression was associated with better overall survival (OS) and leukemia-free survival (LFS) among whole-cohort AML, and independently affected OS determined by Cox repression multivariate analysis. Notably, patients that received hematopoietic stem cell transplantation (HSCT) showed significantly better OS and LFS in DNMT3A lower-expressed groups, whereas patients in DNMT3A higher-expressed groups did not. By bioinformatics analysis, DNMT3A expression was found to be positively correlated with several leukemia-associated genes/microRNAs, and DNMT3A was identified as direct targets of miR-429 and miR-29b in AML. Collectively, our study demonstrated that DNMT3A/3B showed significant expression differences in AML. DNMT3A expression acted as a potential prognostic biomarker and may guide treatment choice between chemotherapy and HSCT in AML.
 ER -

Click to copy this citation from the text box above or download the citation:

Reproductive and hormonal factors and bladder cancer risk: a prospective study and meta-analysis

Xin Xu, Qiwang Mo, Haixiang Shen, Song Wang, Ben Liu,

https://doi.org/10.18632/aging.103523 pp 14691—14698

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu X, Mo Q, Shen H, Wang S, Liu B, . Reproductive and hormonal factors and bladder cancer risk: a prospective study and meta-analysis. . 12:14691-14698. https://doi.org/10.18632/aging.103523

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xu, Xin 
                AU  - Mo, Qiwang 
                AU  - Shen, Haixiang 
                AU  - Wang, Song 
                AU  - Liu, Ben 
                TI  - Reproductive and hormonal factors and bladder cancer risk: a prospective study and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103523
                DO  - 10.18632/aging.103523
                SP  - 14691
                EP  - 14698
                PY  - 
                AB  - Bladder cancer is three to four times more common among men than women. The objectives of this study were to explore the association between reproductive and hormonal factors and risk of bladder cancer among women using data from the Prostate, Lung, Colorectal and Ovarian (PLCO) cohort, and to perform a meta-analysis based on cohort studies. After a median of 11.6 years of follow-up, 237 incident bladder cancer cases were identified in PLCO cohort. Compared with menopause at 50-54 years, earlier menopause (&lt; 45 years) was positively but not significantly associated with bladder cancer risk (HR 1.25, 95% CI 0.91-1.71; p = 0.176). In the meta-analysis, parous women had significantly lower bladder cancer risk than nulliparous women (pooled HR 0.79, 95% CI 0.73-0.86). In addition, menopause at an earlier age was significantly associated with a higher risk of bladder cancer (pooled HR 1.22, 95% CI 1.06-1.40). In conclusion, this study indicated a greater risk in bladder cancer among nulliparous women and among women with early menopause. Further studies are needed to understand the underlying mechanisms.
                ER  -

Click to copy this citation from the text box above or download the citation:

Acetylation-mediated degradation of HSD17B4 regulates the progression of prostate cancer

Huichao Huang, Ruijie Liu, Yahui Huang, Yilu Feng, Ying Fu, Lin Chen, Zhuchu Chen, Yi Cai, Ye Zhang, Yongheng Chen,

https://doi.org/10.18632/aging.103530 pp 14699—14717

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Huang H, Liu R, Huang Y, Feng Y, Fu Y, Chen L, Chen Z, Cai Y, Zhang Y, Chen Y, . Acetylation-mediated degradation of HSD17B4 regulates the progression of prostate cancer. . 12:14699-14717. https://doi.org/10.18632/aging.103530

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Huang, Huichao 
                AU  - Liu, Ruijie 
                AU  - Huang, Yahui 
                AU  - Feng, Yilu 
                AU  - Fu, Ying 
                AU  - Chen, Lin 
                AU  - Chen, Zhuchu 
                AU  - Cai, Yi 
                AU  - Zhang, Ye 
                AU  - Chen, Yongheng 
                TI  - Acetylation-mediated degradation of HSD17B4 regulates the progression of prostate cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103530
                DO  - 10.18632/aging.103530
                SP  - 14699
                EP  - 14717
                PY  - 
                AB  - Steroidogenic enzymes are crucial in prostate cancer (PCa) progression. 17&#x3B2;-Hydroxysteroid dehydrogenase type 4 (HSD17B4), encoded by HSD17B4, lacks catalytic capacity in androgen metabolism. Now the detailed role and molecular mechanism of PCa development are largely unknown. Here we showed that the expression of HSD17B4 was increased in PCa tissues compared to paired paratumor tissues. HSD17B4 knockdown in PCa cells significantly suppressed its proliferation, migration and invasion, while overexpressing HSD17B4 had opposite effects. Mechanistically, we found that the protein level of HSD17B4 was regulated by its acetylation at lysine 669(K669). Dihydroxytestosterone (DHT) treatment increased HSD17B4 acetylation and then promoted its degradation via chaperone-mediated autophagy (CMA). SIRT3 directly interacted with HSD17B4 to inhibit its acetylation and enhance its stability. In addition, we identified CREBBP as a regulator of the K669 acetylation and degradation of HSD17B4, affecting PC cell proliferation, migration and invasion. Notably, in PCa tissues and paired paratumor tissues, the level of HSD17B4 was negatively correlated with its K669 acetylation. Taken together, this study identified a novel role of HSD17B4 in PCa progression and suggested that HSD17B4 and its upstream regulators may be potential therapeutic targets for PCa intervention.
                ER  -

Click to copy this citation from the text box above or download the citation:

Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling

Lei Shi, Guan Sun, Haifeng Zhu,

https://doi.org/10.18632/aging.103531 pp 14718—14735

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Shi L, Sun G, Zhu H, . Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling. . 12:14718-14735. https://doi.org/10.18632/aging.103531

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Shi, Lei 
                AU  - Sun, Guan 
                AU  - Zhu, Haifeng 
                TI  - Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103531
                DO  - 10.18632/aging.103531
                SP  - 14718
                EP  - 14735
                PY  - 
                AB  - Glioma stem cells (GSCs) play an important role in glioblastoma resistance to conventional therapies and disease recurrence. Here, we assessed the therapeutic effect of a demethoxycurcumin analogue, DMC-BH, on GSCs, and investigated the underlying mechanisms. Our in vitro data demonstrate that DMC-BH inhibits GSC proliferation, and induces apoptosis and autophagy in GSCs. In addition, our results show that DMC-BH effectively crosses the blood-brain barrier to inhibit the growth of intracranial GSC tumors in vivo. DMC-BH significantly increased phosphorylation levels of JNK, ERK and c-Jun in GSCs. Inhibition of JNK and ERK activities reversed the pro-apoptotic effect of DMC-BH in GSCs, indicating that the DMC-BH-induced apoptosis in GSCs is mediated via the JNK/ERK signaling pathway. These results suggest that DMC-BH could potentially serve as a effective therapy against GSCs that acts by targeting the JNK/ERK signaling pathway.
                ER  -

Click to copy this citation from the text box above or download the citation:

Prognostic evaluation of esophageal cancer patients with stages I-III

Meng-jun Qiu, Sheng-li Yang, Meng-meng Wang, Ya-nan Li, Xin Jiang, Zao-zao Huang, Zhi-fan Xiong,

https://doi.org/10.18632/aging.103532 pp 14736—14753

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Qiu M, Yang S, Wang M, Li Y, Jiang X, Huang Z, Xiong Z, . Prognostic evaluation of esophageal cancer patients with stages I-III. . 12:14736-14753. https://doi.org/10.18632/aging.103532

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Qiu, Meng-jun 
                AU  - Yang, Sheng-li 
                AU  - Wang, Meng-meng 
                AU  - Li, Ya-nan 
                AU  - Jiang, Xin 
                AU  - Huang, Zao-zao 
                AU  - Xiong, Zhi-fan 
                TI  - Prognostic evaluation of esophageal cancer patients with stages I-III
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103532
                DO  - 10.18632/aging.103532
                SP  - 14736
                EP  - 14753
                PY  - 
                AB  - Purpose: The purpose of this study was to investigate the impact of clinicopathological factors and treatments on the overall survival (OS) and esophageal cancer-specific survival (ECSS) of stages I-III esophageal cancer (EC) patients and to establish a prognostic visual nomogram. Methods: We collected clinical data of patients diagnosed with stages I-III EC without receiving chemotherapy from 2004 to 2014 from the Surveillance, Epidemiology, and End Results (SEER) database. Prognoses were analyzed using the R language software, and nomograms were obtained according to the visual processing logistic regression model, which was verified using the Harrell C-index, receiver operating characteristic (ROC) curve, and calibration curve. Results: A total of 4,305 patients were selected, mostly white males. Most patients were over 60 years old and old age predicted poor prognosis. EC, primarily adenocarcinoma, occurred mostly in the lower third of the esophagus. About half of the patients had T1 (58.00%) and grade II (50.41%) cancer. Of all the patients, 2,448 was treated with surgery and the majority (n = 1,476; 64.85%) of these patients had stage I EC. Stages I-III patients underwent surgery had significantly better OS and ECSS, and endoscopic therapy was associated with the best outcome amongst all the surgical methods. 3.67% of the patients received radiotherapy, predominantly postoperative radiotherapy (2.69%). Older age, squamous cell carcinoma, overlapping lesion of the esophagus, and grades II and III were high-risk factors for poor OS and ECSS for stage I patients, whereas endoscopic therapy, esophagectomy, and esophagectomy with gastrectomy were low-risk factors. Stage II patients with older age, male sex, T3, N1, and grades II and III had shorter OS and ECSS, but patients with any surgical treatment had significantly longer OS and ECSS. T4, N1, and grade III correlated negatively with OS and ECSS in stage III patients, and any surgical treatment correlated positively with longer OS and ECSS. The OS and ECSS rates of stages I-III EC patients with a total score of more than 150 points in the nomogram were both only 40% after 3 years and 30% after 5 years. The C-index, ROC curve, and calibration curve indicated that the nomograms established in this study were suitable to assess patient prognosis. Conclusion: The nomogram established in this study is an effective clinical tool to predict the prognosis of stages I-III EC patients without chemotherapy.
                ER  -

Click to copy this citation from the text box above or download the citation:

Silencing DSCAM-AS1 suppresses the growth and invasion of ER-positive breast cancer cells by downregulating both DCTPP1 and QPRT

Zhang Yue, Jia Shusheng, Song Hongtao, Zhao Shu, Huang Lan, Zhang Qingyuan, Cheng Shaoqiang, Huang Yuanxi,

https://doi.org/10.18632/aging.103538 pp 14754—14774

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Yue Z, Shusheng J, Hongtao S, Shu Z, Lan H, Qingyuan Z, Shaoqiang C, Yuanxi H, . Silencing DSCAM-AS1 suppresses the growth and invasion of ER-positive breast cancer cells by downregulating both DCTPP1 and QPRT. . 12:14754-14774. https://doi.org/10.18632/aging.103538

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Yue, Zhang 
                AU  - Shusheng, Jia 
                AU  - Hongtao, Song 
                AU  - Shu, Zhao 
                AU  - Lan, Huang 
                AU  - Qingyuan, Zhang 
                AU  - Shaoqiang, Cheng 
                AU  - Yuanxi, Huang 
                TI  - Silencing DSCAM-AS1 suppresses the growth and invasion of ER-positive breast cancer cells by downregulating both DCTPP1 and QPRT
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103538
                DO  - 10.18632/aging.103538
                SP  - 14754
                EP  - 14774
                PY  - 
                AB  - Breast cancer (BC) remains a significant threat to the health of women; however, the mechanism underlying the initiation and progression of BC is poorly understood. We analyzed data from the Gene Expression Omnibus database and The Cancer Genome Atlas datasets to identify differentially expressed genes between BC and normal tissues. The roles of dCTP pyrophosphatase 1 (DCTPP1) and quinolinate phosphoribosyltransferase (QPRT) in BC cells were investigated after knocking down or overexpressing the genes. The regulatory effects of Down syndrome cell adhesion molecule antisense RNA 1 (DSCAM-AS1) on DCTPP1 and QPRT expression were determined using luciferase reporter, RNA immunoprecipitation, RNA pull-down, chromatin immunoprecipitation, and fluorescence in situ hybridization assays. DCTPP1 and QPRT were overexpressed in BC compared to normal tissues. Overexpression of DCTPP1 and QPRT was associated with poor BC progression and promoted growth, migration, and invasion of MCF7 and T47D cells but inhibited apoptosis. DSCAM-AS1 increased QPRT expression via competitively binding miRNA-150-5p and miRNA-2467-3p. DSCAM-AS1 promoted DCTPP1 gene transcription by affecting H3K27 acetylation and enhanced DCTPP1 mRNA stability by binding to the 3&#x2032; untranslated region, which collectively resulted in DCTPP1 overexpression. Overall, DSCAM-AS1 knockdown decreased both DCTPP1 and QPRT expression, inhibiting the growth, migration, and invasion of estrogen receptor-positive BC.
                ER  -

Click to copy this citation from the text box above or download the citation:

The circular RNA circEIF3M promotes breast cancer progression by promoting cyclin D1 expression

Xiujuan Li, Zhaojun Ren, Yufeng Yao, Jun Bao, Qiao Yu,

https://doi.org/10.18632/aging.103539 pp 14775—14790

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li X, Ren Z, Yao Y, Bao J, Yu Q, . The circular RNA circEIF3M promotes breast cancer progression by promoting cyclin D1 expression. . 12:14775-14790. https://doi.org/10.18632/aging.103539

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Xiujuan 
                AU  - Ren, Zhaojun 
                AU  - Yao, Yufeng 
                AU  - Bao, Jun 
                AU  - Yu, Qiao 
                TI  - The circular RNA circEIF3M promotes breast cancer progression by promoting cyclin D1 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103539
                DO  - 10.18632/aging.103539
                SP  - 14775
                EP  - 14790
                PY  - 
                AB  - We investigated the function of circular RNA circEIF3M (hsa_circ_0003119) in triple-negative breast cancer. The expression profiles of circRNAs in 3 specimens of triple-negative breast cancer tissues with adjacent nontumor tissues were analyzed by RNA-sequencing. We verified the oncogenic role of circEIF3M in triple-negative breast cancer through a series of biological function experiments. It was found that circEIF3M was markedly upregulated in triple-negative breast cancer as compared to adjacent nontumor tissue, and that circEIF3M promoted triple-negative breast cancer cell proliferation, migration, and invasion. Mechanistic analysis indicated that circEIF3M may act as a competing endogenous RNA for miR-33a that relieves the inhibitory effect of miR-33a on its target cyclin D1. These findings showed that circEIF3M promotes triple-negative breast cancer progression via the circEIF3M/ miR-33a/ cyclin D1 axis.
                ER  -

Click to copy this citation from the text box above or download the citation:

MiR-185 targets POT1 to induce telomere dysfunction and cellular senescence

Tingting Li, Zhenhua Luo, Song Lin, Chujun Li, Shenkun Dai, Haoli Wang, Junjiu Huang, Wenbin Ma, Zhou Songyang, Yan Huang,

https://doi.org/10.18632/aging.103541 pp 14791—14807

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li T, Luo Z, Lin S, Li C, Dai S, Wang H, Huang J, Ma W, Songyang Z, Huang Y, . MiR-185 targets POT1 to induce telomere dysfunction and cellular senescence. . 12:14791-14807. https://doi.org/10.18632/aging.103541

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Tingting 
                AU  - Luo, Zhenhua 
                AU  - Lin, Song 
                AU  - Li, Chujun 
                AU  - Dai, Shenkun 
                AU  - Wang, Haoli 
                AU  - Huang, Junjiu 
                AU  - Ma, Wenbin 
                AU  - Songyang, Zhou 
                AU  - Huang, Yan 
                TI  - MiR-185 targets POT1 to induce telomere dysfunction and cellular senescence
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103541
                DO  - 10.18632/aging.103541
                SP  - 14791
                EP  - 14807
                PY  - 
                AB  - Protection of telomere 1 (POT1), the telomeric single-stranded DNA (ssDNA)-binding protein in the shelterin complex, has been implicated in the DNA damage response, tumorigenesis and aging. Telomere dysfunction induced by telomere deprotection could accelerate cellular senescence in primary human cells. While previous work demonstrated the biological mechanism of POT1 in aging and cancer, how POT1 is posttranscriptionally regulated remains largely unknown. To better understand the POT1 regulatory axis, we performed bioinformatic prediction, and selected candidates were further confirmed by dual-luciferase reporter assay. Collectively, our results revealed that miR-185 can significantly reduce POT1 mRNA and protein levels by directly targeting the POT1 3&#x2019;-untranslated region (3&#x2019;-UTR). Overexpression of miR-185 increased telomere dysfunction-induced foci (TIF) signals in both cancer cells and primary human fibroblasts. Elevated miR-185 led to telomere elongation in the telomerase-positive cell line HTC75, which was phenotypically consistent with POT1 knocking down. Moreover, miR-185 accelerated the replicative senescence process in primary human fibroblasts in a POT1-dependent manner. Interestingly, increased serum miR-185 could represent a potential aging-related biomarker. Taken together, our findings reveal miR-185 as a novel aging-related miRNA that targets POT1 and provide insight into the telomere and senescence regulatory network at both the intracellular and extracellular levels.
                ER  -

Click to copy this citation from the text box above or download the citation:

Hsa_circ_0044226 knockdown attenuates progression of pulmonary fibrosis by inhibiting CDC27

Fei Qi, Yong Li, Xue Yang, Yanping Wu, Lianjun Lin, Xinmin Liu,

https://doi.org/10.18632/aging.103543 pp 14808—14818

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Qi F, Li Y, Yang X, Wu Y, Lin L, Liu X, . Hsa_circ_0044226 knockdown attenuates progression of pulmonary fibrosis by inhibiting CDC27. . 12:14808-14818. https://doi.org/10.18632/aging.103543

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Qi, Fei 
                AU  - Li, Yong 
                AU  - Yang, Xue 
                AU  - Wu, Yanping 
                AU  - Lin, Lianjun 
                AU  - Liu, Xinmin 
                TI  - Hsa_circ_0044226 knockdown attenuates progression of pulmonary fibrosis by inhibiting CDC27
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103543
                DO  - 10.18632/aging.103543
                SP  - 14808
                EP  - 14818
                PY  - 
                AB  - Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disorder. Here, we performed a bioinformatics analysis using the GSE102660 dataset from the Gene Expression Omnibus database to identify differentially expressed circRNAs (DEcircRNAs) in tissues from IPF patients and healthy controls. The results identified 45 DEcircRNAs, among which expression of hsa_circ_0044226 was markedly higher in lung tissues from IPF patients than from healthy controls. Knocking down hsa_circ_0044226 expression using a targeted shRNA inhibited TGF-&#x3B2;1-induced fibrosis in RLE-6TN cells and in a bleomycin-induced mouse model of IPA. The diminished TGF-&#x3B2;1-induced fibrosis was associated with upregulated expression of E-cadherin and downregulated expression of &#x3B1;-SMA, collagen III and fibronectin 1, as well as with reduced expression of CDC27, suggesting inhibition of epithelial-to-mesenchymal transition (EMT). All of those effects were reversed by overexpression of CDC27. This suggests CDC27 overexpression abolishes the antifibrotic effect of hsa_circ_0044226 knockdown through activation of EMT. Furthermore, hsa_circ_0044226 knockdown decreased the expression of CDC27 in BLM-induced pulmonary fibrosis mouse model. Collectively then, these findings indicate that downregulation of hsa_circ_0044226 attenuates pulmonary fibrosis in vitro and in vivo by inhibiting CDC27, which in turn suppresses EMT. This suggests hsa_circ_0044226 may be a useful therapeutic target for the treatment of IPF.
                ER  -

Click to copy this citation from the text box above or download the citation:

ACE2 activator diminazene aceturate ameliorates Alzheimer's disease-like neuropathology and rescues cognitive impairment in SAMP8 mice

Rui Duan, Xiao Xue, Qiao-Quan Zhang, Si-Yu Wang, Peng-Yu Gong, Yan E, Teng Jiang, Ying-Dong Zhang,

https://doi.org/10.18632/aging.103544 pp 14819—14829

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Duan R, Xue X, Zhang Q, Wang S, Gong P, E Y, Jiang T, Zhang Y, . ACE2 activator diminazene aceturate ameliorates Alzheimer's disease-like neuropathology and rescues cognitive impairment in SAMP8 mice. . 12:14819-14829. https://doi.org/10.18632/aging.103544

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Duan, Rui 
                AU  - Xue, Xiao 
                AU  - Zhang, Qiao-Quan 
                AU  - Wang, Si-Yu 
                AU  - Gong, Peng-Yu 
                AU  - E, Yan 
                AU  - Jiang, Teng 
                AU  - Zhang, Ying-Dong 
                TI  - ACE2 activator diminazene aceturate ameliorates Alzheimer's disease-like neuropathology and rescues cognitive impairment in SAMP8 mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103544
                DO  - 10.18632/aging.103544
                SP  - 14819
                EP  - 14829
                PY  - 
                AB  - Previously, we revealed that brain Ang-(1-7) deficiency was involved in the pathogenesis of sporadic Alzheimer&#x2019;s disease (AD). We speculated that restoration of brain Ang-(1-7) levels might have a therapeutic effect against AD. However, the relatively short duration of biological effect limited the application of Ang-(1-7) in animal experiments. Since Ang-(1-7) is generated by its metabolic enzyme ACE2, we then tested the efficacy of an ACE2 activator diminazene aceturate (DIZE) on AD-like neuropathology and cognitive impairment in senescence-accelerated mouse prone substrain 8 (SAMP8) mice, an animal model of sporadic AD. Eight-month-old SAMP8 mice were injected intraperitoneally with vehicle or DIZE once a day for 30 consecutive days. DIZE markedly elevated brain Ang-(1-7) and MAS1 levels. Meanwhile, DIZE significantly reduced the levels of A&#x3B2;1-42, hyperphosphorylated tau and pro-inflammatory cytokines in the brain. The synaptic and neuronal losses in the brain were ameliorated by DIZE. Importantly, DIZE improved spatial cognitive functions in the Morris water maze test. In conclusion, this study demonstrates that DIZE ameliorates AD-like neuropathology and rescues cognitive impairment in SAMP8 mice. These beneficial effects of DIZE may be achieved by activating brain ACE2/Ang-(1-7)/MAS1 axis. These findings highlight brain ACE2/Ang-(1-7)/MAS1 axis as a potential target for the treatment of sporadic AD.
                ER  -

Click to copy this citation from the text box above or download the citation:

FGF2-induced PI3K/Akt signaling evokes greater proliferation and adipogenic differentiation of human adipose stem cells from breast than from abdomen or thigh

Guan-Ming Lu, Yong-Xian Rong, Zhi-Jie Liang, Dong-Lin Hunag, Fang-Xiao Wu, Yan-Fei Ma, Zhi-Zhai Luo, Xin-Heng Liu, Steven Mo, Hong-Mian Li,

https://doi.org/10.18632/aging.103547 pp 14830—14848

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lu G, Rong Y, Liang Z, Hunag D, Wu F, Ma Y, Luo Z, Liu X, Mo S, Li H, . FGF2-induced PI3K/Akt signaling evokes greater proliferation and adipogenic differentiation of human adipose stem cells from breast than from abdomen or thigh. . 12:14830-14848. https://doi.org/10.18632/aging.103547

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lu, Guan-Ming 
                AU  - Rong, Yong-Xian 
                AU  - Liang, Zhi-Jie 
                AU  - Hunag, Dong-Lin 
                AU  - Wu, Fang-Xiao 
                AU  - Ma, Yan-Fei 
                AU  - Luo, Zhi-Zhai 
                AU  - Liu, Xin-Heng 
                AU  - Mo, Steven 
                AU  - Li, Hong-Mian 
                TI  - FGF2-induced PI3K/Akt signaling evokes greater proliferation and adipogenic differentiation of human adipose stem cells from breast than from abdomen or thigh
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103547
                DO  - 10.18632/aging.103547
                SP  - 14830
                EP  - 14848
                PY  - 
                AB  - In this study, human adipose stem cells were isolated from subcutaneous fat in the thigh (htASCs), abdomen (haASCs) and breast (hbASCs). Flow cytometry was used to detect cell surface markers, and an enzyme-linked immunosorbent assay was used to detect paracrine activity. Paracrine gene expression in the three cell types was examined using real-time qPCR, and adipogenic ability was assessed using Oil Red O staining. RNA from third-passage haASCs and hbASCs was sequenced. The results showed that the differentiation potential marker markers CD49d and CD54 were similar across hbASCs from 10 subjects. The hbASCs showed higher colony forming ability and expression of fibroblast growth factor-2, tissue inhibitor of metalloproteinase-1 and stromal cell derived factor-1 than htASCs and haASCs. Stimulating hbASCs with FGF2 promoted adipogenic differentiation, while treating the cells with the PI3K inhibitor LY294002 inhibited differentiation. These results suggest that the PI3K/Akt signaling pathway can promote proliferation and adipogenic differentiation of adipose stem cells, and that activation of this pathway by FGF2 may explain why hbASCs show greater proliferation and adipogenic differentiation than haASCs and htASCs.
                ER  -

Click to copy this citation from the text box above or download the citation:

Targeting CCL20 inhibits subarachnoid hemorrhage-related neuroinflammation in mice

Li-Shang Liao, Ming-Wei Zhang, Ying-Jiang Gu, Xiao-Chuan Sun,

https://doi.org/10.18632/aging.103548 pp 14849—14862

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liao L, Zhang M, Gu Y, Sun X, . Targeting CCL20 inhibits subarachnoid hemorrhage-related neuroinflammation in mice. . 12:14849-14862. https://doi.org/10.18632/aging.103548

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liao, Li-Shang 
                AU  - Zhang, Ming-Wei 
                AU  - Gu, Ying-Jiang 
                AU  - Sun, Xiao-Chuan 
                TI  - Targeting CCL20 inhibits subarachnoid hemorrhage-related neuroinflammation in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103548
                DO  - 10.18632/aging.103548
                SP  - 14849
                EP  - 14862
                PY  - 
                AB  - Recent evidence suggests that CC chemokine ligand 20 (CCL20) is upregulated after subarachnoid hemorrhage (SAH). Here, we investigated the functions of CCL20 in SAH injury and its underlying mechanisms of action. We found that CCL20 is upregulated in an SAH mouse model and in cultured primary microglia and neurons. CCL20-neutralizing antibody alleviated SAH-induced neurological deficits, decreased brain water content and neuronal apoptosis, and repressed microglial activation. We observed increased levels of CCL20, CC chemokine receptor 6 (CCR6), interleukin 1 beta (IL-1&#x3B2;), and tumor necrosis factor alpha (TNF-&#x3B1;), as well as of microglial activation in microglia treated with oxyhemoglobin (OxyHb). CCL20 or CCR6 knockdown reversed the effects of OxyHb on microglia. Conditioned medium from OxyHb-treated microglia induced neuronal apoptosis, while the percentage of apoptotic neurons in the conditioned medium from microglia transfected with CCL20 siRNA or CCR6 siRNA was decreased. We observed no decrease in OxyHb-induced apoptosis in CCL20-knockdown neurons. Conditioned medium from OxyHb-treated neurons led to microglial activation and induced CCR6, IL-1&#x3B2; and TNF-&#x3B1; expression, while CCL20 knockdown in neurons or CCR6 knockdown in microglia reversed those effects. Our results thus suggest CCL20 may be targeted to elicit therapeutic benefits after SAH injury.
                ER  -

Click to copy this citation from the text box above or download the citation:

Comprehensive analysis of m6A regulators prognostic value in prostate cancer

Guangjie Ji, Cong Huang, Shiming He, Yanqing Gong, Gang Song, Xuesong Li, Liqun Zhou,

https://doi.org/10.18632/aging.103549 pp 14863—14884

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ji G, Huang C, He S, Gong Y, Song G, Li X, Zhou L, . Comprehensive analysis of m6A regulators prognostic value in prostate cancer. . 12:14863-14884. https://doi.org/10.18632/aging.103549

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ji, Guangjie 
                AU  - Huang, Cong 
                AU  - He, Shiming 
                AU  - Gong, Yanqing 
                AU  - Song, Gang 
                AU  - Li, Xuesong 
                AU  - Zhou, Liqun 
                TI  - Comprehensive analysis of m6A regulators prognostic value in prostate cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103549
                DO  - 10.18632/aging.103549
                SP  - 14863
                EP  - 14884
                PY  - 
                AB  - Background: N6-methyladenosine (m6A) is the most prevalent RNA modification. While the role of m6A in prostate cancer remains unknown. We aim to measure the effects of m6A methylation regulatory genes during the development and progression of prostate cancer.Methods: We collected transcriptome information and gene-level alteration data from The Cancer Genome Atlas datasets. The log-rank test and Cox regression model were used to examine the prognosis value of m6A methylation regulatory genes of prostate cancer.Results: We discovered that most of m6A methylation regulators were highly expressed in aggressive prostate cancer. Univariable and multivariable Cox regression results showed that the expression of Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) and N6-adenosine-methyltransferase non-catalytic subunit (METTL14) and copy number variant of AlkB Homolog 5 (ALKBH5) were considerably associated with a recurrence-free survival of prostate cancer. Furthermore, a high level of m6A methylation in mRNA promotes the progression of prostate cancer via regulating subcellular protein localization.Conclusion: Patients with a high level of mRNA methylation resulted from overexpression of reader proteins and methyltransferase complexes had poor survival benefits through influencing protein subcellular location in prostate cancer.
                ER  -

Click to copy this citation from the text box above or download the citation:

Circular RNA DHX33 promotes malignant behavior in ccRCC by targeting miR-489-3p/MEK1 axis

Jie Wang, Jian-Qiu Zhang, Xiao-Lei Zhao, Jing-Yu Lu, Ze-Ming Weng, Zhen-Min Ding, Feng-Qiang Yang,

https://doi.org/10.18632/aging.103550 pp 14885—14896

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang J, Zhang J, Zhao X, Lu J, Weng Z, Ding Z, Yang F, . Circular RNA DHX33 promotes malignant behavior in ccRCC by targeting miR-489-3p/MEK1 axis. . 12:14885-14896. https://doi.org/10.18632/aging.103550

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Jie 
                AU  - Zhang, Jian-Qiu 
                AU  - Zhao, Xiao-Lei 
                AU  - Lu, Jing-Yu 
                AU  - Weng, Ze-Ming 
                AU  - Ding, Zhen-Min 
                AU  - Yang, Feng-Qiang 
                TI  - Circular RNA DHX33 promotes malignant behavior in ccRCC by targeting miR-489-3p/MEK1 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103550
                DO  - 10.18632/aging.103550
                SP  - 14885
                EP  - 14896
                PY  - 
                AB  - Mounting evidence indicates that circular RNAs modulate the initiation of clear cell renal cell carcinoma (ccRCC). However, their specific roles in the malignancy of ccRCC is understudied. Here, we present a novel circular RNA, circDHX33, that is up-regulated in ccRCC cell lines and tissues. Upregulated circDHX33 in ccRCC patients significantly correlates with advanced TNM stage and metastasis. Suppressing circDHX33 expression inhibits the proliferation and invasion of cultured cells, and suppresses tumor growth in vivo. Mechanistically, we show that circDHX33 promotes ccRCC progression by sponging miR-489-3p and modulating MEK1 expression. In conclusion, our findings suggest that circDHX33 plays a role in promoting ccRCC via the miR-489-3p/MEK1 axis and may serve as a novel therapeutic target for the treatment of ccRCC patients
                ER  -

Click to copy this citation from the text box above or download the citation:

Neuroprotective and neurogenic effects of novel tetramethylpyrazine derivative T-006 in Parkinson’s disease models through activating the MEF2-PGC1α and BDNF/CREB pathways

Haiyun Chen, Jie Cao, Ling Zha, Peile Wang, Zheng Liu, Baojian Guo, Gaoxiao Zhang, Yewei Sun, Zaijun Zhang, Yuqiang Wang,

https://doi.org/10.18632/aging.103551 pp 14897—14917

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen H, Cao J, Zha L, Wang P, Liu Z, Guo B, Zhang G, Sun Y, Zhang Z, Wang Y, . Neuroprotective and neurogenic effects of novel tetramethylpyrazine derivative T-006 in Parkinson’s disease models through activating the MEF2-PGC1α and BDNF/CREB pathways. . 12:14897-14917. https://doi.org/10.18632/aging.103551

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Haiyun 
                AU  - Cao, Jie 
                AU  - Zha, Ling 
                AU  - Wang, Peile 
                AU  - Liu, Zheng 
                AU  - Guo, Baojian 
                AU  - Zhang, Gaoxiao 
                AU  - Sun, Yewei 
                AU  - Zhang, Zaijun 
                AU  - Wang, Yuqiang 
                TI  - Neuroprotective and neurogenic effects of novel tetramethylpyrazine derivative T-006 in Parkinson’s disease models through activating the MEF2-PGC1α and BDNF/CREB pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103551
                DO  - 10.18632/aging.103551
                SP  - 14897
                EP  - 14917
                PY  - 
                AB  - T-006, a new derivative of tetramethylpyrazine, has been recently found to protect against 6-hydroxydopamine (6-OHDA)-induced neuronal damage and clear &#x3B1;-synuclein (&#x3B1;-syn) by enhancing proteasome activity in an &#x3B1;-syn transgenic Parkinson&#x2019;s disease (PD) model. The effect of T-006 on the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced PD model, however, has not been tested and T-006&#x2019;s neuroprotective mechanisms have not been fully elucidated. In this study, we further investigated the neuroprotective and neurogenic effects of T-006 and explored its underlying mechanism of action in both cellular and animal PD models. T-006 was able to improve locomotor behavior, increase survival of nigra dopaminergic neurons and boost striatal dopamine levels in both MPTP- and 6-OHDA-induced animals. T-006 treatment restored the altered expressions of myocyte enhancer factor 2D (MEF2D), peroxisome proliferator-activated receptor &#x3B3; (PPAR&#x3B3;) co-activator 1&#x3B1; (PGC1&#x3B1;) and NF-E2-related factor 1/2 (Nrf1/2) via modulation of Akt/GSK3&#x3B2; signaling. T-006 stimulated MEF2, PGC1&#x3B1; and Nrf2 transcriptional activities, inducing Nrf2 nuclear localization. Interestingly, T-006 promoted endogenous adult neurogenesis toward a dopaminergic phenotype by activating brain-derived neurotrophic factor (BDNF) and cAMP responsive element-binding protein (CREB) in 6-OHDA rats. Our work demonstrated that T-006 is a potent neuroprotective and neuroregenerative agent that may have therapeutic potential in the treatment of PD.
                ER  -

Click to copy this citation from the text box above or download the citation:

RP11-295G20.2 facilitates hepatocellular carcinoma progression via the miR-6884-3p/CCNB1 pathway

Jing Li, Tingting Xia, Junyan Cao, Donghong He, Zhaocong Chen, Biao Liang, Jie Song,

https://doi.org/10.18632/aging.103552 pp 14918—14932

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li J, Xia T, Cao J, He D, Chen Z, Liang B, Song J, . RP11-295G20.2 facilitates hepatocellular carcinoma progression via the miR-6884-3p/CCNB1 pathway. . 12:14918-14932. https://doi.org/10.18632/aging.103552

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Jing 
                AU  - Xia, Tingting 
                AU  - Cao, Junyan 
                AU  - He, Donghong 
                AU  - Chen, Zhaocong 
                AU  - Liang, Biao 
                AU  - Song, Jie 
                TI  - RP11-295G20.2 facilitates hepatocellular carcinoma progression via the miR-6884-3p/CCNB1 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103552
                DO  - 10.18632/aging.103552
                SP  - 14918
                EP  - 14932
                PY  - 
                AB  - Objective: An increasing number of studies have indicated that long noncoding RNAs (lncRNAs) play an important role in the pathogenesis of hepatocellular carcinoma (HCC). In this study, we aimed to clarify the roles of RP11-295G20.2 in HCC progression and the underlying molecular mechanisms.Results: Bioinformatics analyses based TCGA data suggested that RP11-295G20.2 was significantly upregulated in HCC tissues and increased RP11-295G20.2 expression level correlated with poor overall survival of patients with HCC. The results of RT-PCR further showed that RP11-295G20.2 was upregulated in HCC tissues and cell lines. Functionally, RP11-295G20.2 knockdown significantly inhibited the proliferation, colony formation, invasion and migration, but induced the apoptosis of HCC cells. In line with this, downregulation of RP11-295G20.2 in HCC lines markedly suppressed the tumor growth in vivo. Mechanistically, RP11-295G20.2 could upregulate CCNB1 through targeting miR-6884-3p. More importantly, our rescue experiments revealed that miR-6884-3p/CCNB1 axis was involved in RP11-295G20.2-meditated tumorigenic behaviors of HCC cells.Conclusions: RP11-295G20.2 can contribute to HCC progression at least partly via the miR-6884-3p/CCNB1 axis, suggesting that RP11-295G20.2 may be a potential target for HCC therapy.Methods: RT-qPCR was employed to examine the expression levels of RP11-295G20.2, miR-6884-3p, and CCNB1 in HCC tissues and cell lines. CCK8 assay, transwell assay, colony formation assay and flow cytometry analysis were performed to evaluate the biological function of RP11-295G20.2 in HCC cells. The xenograft tumor assay was used to assess the effect of RP11-295G20.2 on the in vivo growth of HCC cells. The luciferase reporter assay, RIP assay and Spearman&apos;s correlation analysis were performed to explore the potential mechanisms underlying the roles of RP11-295G20.2 in HCC progression.
                ER  -

Click to copy this citation from the text box above or download the citation:

A new survival model based on ferroptosis-related genes for prognostic prediction in clear cell renal cell carcinoma

Guangzhen Wu, Qifei Wang, Yingkun Xu, Quanlin Li, Liang Cheng,

https://doi.org/10.18632/aging.103553 pp 14933—14948

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wu G, Wang Q, Xu Y, Li Q, Cheng L, . A new survival model based on ferroptosis-related genes for prognostic prediction in clear cell renal cell carcinoma. . 12:14933-14948. https://doi.org/10.18632/aging.103553

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wu, Guangzhen 
                AU  - Wang, Qifei 
                AU  - Xu, Yingkun 
                AU  - Li, Quanlin 
                AU  - Cheng, Liang 
                TI  - A new survival model based on ferroptosis-related genes for prognostic prediction in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103553
                DO  - 10.18632/aging.103553
                SP  - 14933
                EP  - 14948
                PY  - 
                AB  - In this study, we analyzed the clinical significance of ferroptosis-related genes (FRGs) in 32 cancer types in the GSCA database. We detected a 2-82% mutation rate among 36 FRGs. In clear cell renal cell carcinoma (ccRCC; n=539) tissues from the The Cancer Genome Atlas database, 30 of 36 FRGs were differentially expressed (up- or down-regulated) compared to normal kidney tissues (n=72). Consensus clustering analysis identified two clusters of FRGs based on similar co-expression in ccRCC tissues. We then used LASSO regression analysis to build a new survival model based on five risk-related FRGs (CARS, NCOA4, FANCD2, HMGCR, and SLC7A11). Receiver operating characteristic curve analysis confirmed good prognostic performance of the new survival model with an area under the curve of 0.73. High FANCD2, CARS, and SLC7A11 expression and low HMGCR and NCOA4 expression were associated with high-risk ccRCC patients. Multivariate analysis showed that risk score, age, stage, and grade were independent risk factors associated with prognosis in ccRCC. These findings demonstrate that this five risk-related FRG-based survival model accurately predicts prognosis in ccRCC patients, and suggest FRGs are potential prognostic biomarkers and therapeutic targets in several cancer types.
                ER  -

Click to copy this citation from the text box above or download the citation:

Analysis of plasma metabolic profile, characteristics and enzymes in the progression from chronic hepatitis B to hepatocellular carcinoma

Fei-Fei Cai, Ya-Nan Song, Yi-Yu Lu, Yongyu Zhang, Yi-Yang Hu, Shi-Bing Su,

https://doi.org/10.18632/aging.103554 pp 14949—14965

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Cai F, Song Y, Lu Y, Zhang Y, Hu Y, Su S, . Analysis of plasma metabolic profile, characteristics and enzymes in the progression from chronic hepatitis B to hepatocellular carcinoma. . 12:14949-14965. https://doi.org/10.18632/aging.103554

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Cai, Fei-Fei 
                AU  - Song, Ya-Nan 
                AU  - Lu, Yi-Yu 
                AU  - Zhang, Yongyu 
                AU  - Hu, Yi-Yang 
                AU  - Su, Shi-Bing 
                TI  - Analysis of plasma metabolic profile, characteristics and enzymes in the progression from chronic hepatitis B to hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103554
                DO  - 10.18632/aging.103554
                SP  - 14949
                EP  - 14965
                PY  - 
                AB  - Hepatitis B virus (HBV) infection is an important factor causing hepatocellular carcinoma (HCC). The aim of this study was to investigate the metabolic characteristics and related metabolic enzyme changes during the progression from chronic hepatitis B (CHB) to liver cirrhosis (LC) and, ultimately, to HCC. An untargeted metabolomics assay was performed in plasma from 50 healthy volunteers, 43 CHB patients, 67 LC patients, and 39 HCC patients. A total of 24 differential metabolites (DMs) were identified. Joint pathway analysis suggested striking changes in amino acid metabolism and lipid metabolism from CHB to HCC. The panel of L-serine, creatine and glycine distinguished LC from CHB, and L-serine, cystathionine, creatine and linoleic acid distinguished HCC from LC. Bioinformatic analysis of publicly available data showed that differential metabolite profile-associated enzyme genes, including alanine-glyoxylate aminotransferase-2 (AGXT2), D-amino-acid oxidase (DAO), and cystathionine gamma-lyase (CTH), were downregulated, while bisphosphoglycerate mutase (BPGM), cystathionine-&#x3B2;-synthase (CBS), phosphoserine phosphatase (PSPH) and acyl-CoA thioesterase 7 (ACOT7) were upregulated, in HCC, all of which correlated with a poor prognosis for HCC patients. Our results indicated that serum metabolites and related enzymes are of considerable significance for the diagnosis and prognosis of HCC and can provide a theoretical basis and therapeutic index for future diagnosis and treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis

Yujin Liu, Feng Zhu, Huarong Li, Heng Fan, Hui Wu, Yalan Dong, Si Chu, Chen Tan, Quansheng Wang, Hongxia He, Fei Gao, Xueyuan Leng, Qiaoli Zhou, Xiwen Zhu,

https://doi.org/10.18632/aging.103555 pp 14966—14977

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liu Y, Zhu F, Li H, Fan H, Wu H, Dong Y, Chu S, Tan C, Wang Q, He H, Gao F, Leng X, Zhou Q, et al, . MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis. . 12:14966-14977. https://doi.org/10.18632/aging.103555

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liu, Yujin 
                AU  - Zhu, Feng 
                AU  - Li, Huarong 
                AU  - Fan, Heng 
                AU  - Wu, Hui 
                AU  - Dong, Yalan 
                AU  - Chu, Si 
                AU  - Tan, Chen 
                AU  - Wang, Quansheng 
                AU  - He, Hongxia 
                AU  - Gao, Fei 
                AU  - Leng, Xueyuan 
                AU  - Zhou, Qiaoli 
                AU  - Zhu, Xiwen 
                TI  - MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103555
                DO  - 10.18632/aging.103555
                SP  - 14966
                EP  - 14977
                PY  - 
                AB  - Intestinal barrier dysfunction is a hallmark of inflammatory bowel disease (IBD). MiR-155 is increased in colitis and downregulates expression of hypoxia-inducible factor 1&#x3B1; (HIF-1&#x3B1;). Here, we investigated the effects of miR-155 on intestinal barrier dysfunction in dextran sulfate sodium (DSS)-induced colitis. We found that miR-155 antagomir treatment relieved weight loss and intestinal damage in IBD mouse models (P &lt; 0.05). Furthermore, electron microscopy and immunofluorescence imaging showed that miR-155 increased intestinal barrier dysfunction and downregulated the expression of tight junction proteins in DSS-induced colitis. FG-4497, which upregulates HIF-1&#x3B1; expression, elicited protective effects on the intestinal barrier in DSS-induced colitis. Dual luciferase reporter assays also confirmed that miR-155 downregulated expression of HIF-1&#x3B1;. Finally, we discovered that HIF-1&#x3B1; levels were elevated by miR-155 antagomir treatment (P &lt; 0.05) and that TFF-3 expression correlated positively with HIF-1&#x3B1; expression. These results suggest that miR-155 contributes to DSS-induced colitis by promoting intestinal barrier dysfunction and inhibiting the HIF-1&#x3B1;/TFF-3 axis.
                ER  -

Click to copy this citation from the text box above or download the citation:

Inhibition of miRNA-152-3p enhances diabetic wound repair via upregulation of PTEN

Yan Xu, Tao Yu, Lei He, Liu Ouyang, Yanzhen Qu, Junjie Zhou, Yu Han, Deyu Duan,

https://doi.org/10.18632/aging.103557 pp 14978—14989

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu Y, Yu T, He L, Ouyang L, Qu Y, Zhou J, Han Y, Duan D, . Inhibition of miRNA-152-3p enhances diabetic wound repair via upregulation of PTEN. . 12:14978-14989. https://doi.org/10.18632/aging.103557

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xu, Yan 
                AU  - Yu, Tao 
                AU  - He, Lei 
                AU  - Ouyang, Liu 
                AU  - Qu, Yanzhen 
                AU  - Zhou, Junjie 
                AU  - Han, Yu 
                AU  - Duan, Deyu 
                TI  - Inhibition of miRNA-152-3p enhances diabetic wound repair via upregulation of PTEN
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103557
                DO  - 10.18632/aging.103557
                SP  - 14978
                EP  - 14989
                PY  - 
                AB  - Diabetic foot ulcer (DFU) is a major complication of diabetes in the elderly population. The aim of this study was to investigate the potential mechanism of DFU at the molecular level and explore a feasible therapy for it. Using data from the Gene Expression Omnibus (GEO) database, we found that phosphatase and tensin homolog (PTEN) is differentially expressed between diabetic patients and those without diabetes. We also found that PTEN expression is regulated by glucose stimulation. In addition, decreased function of human umbilical vein endothelial cells (HUVECs) was found to be associated with reduction of PTEN. We identified microRNA-152-3p (miR-152-3p) to be a putative upstream negative regulator of PTEN, and in vivo and in vitro results indicated that miR-152-3p antagonist could restore HUVEC function and accelerate wound repair. Thus, miR-152-3p-induced downregulation of PTEN appears responsible for the delayed wound healing in DFU, and miR-152-3p inhibition may effectively accelerate wound repair, thereby providing a potential target for DFU therapy.
                ER  -

Click to copy this citation from the text box above or download the citation:

Lysine-specific histone demethylase 1B (LSD2/KDM1B) represses p53 expression to promote proliferation and inhibit apoptosis in colorectal cancer through LSD2-mediated H3K4me2 demethylation

Shaoxin Cai, Jinsi Wang, Wei Zeng, Xuefei Cheng, Lihang Liu, Weihua Li,

https://doi.org/10.18632/aging.103558 pp 14990—15001

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Cai S, Wang J, Zeng W, Cheng X, Liu L, Li W, . Lysine-specific histone demethylase 1B (LSD2/KDM1B) represses p53 expression to promote proliferation and inhibit apoptosis in colorectal cancer through LSD2-mediated H3K4me2 demethylation. . 12:14990-15001. https://doi.org/10.18632/aging.103558

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Cai, Shaoxin 
                AU  - Wang, Jinsi 
                AU  - Zeng, Wei 
                AU  - Cheng, Xuefei 
                AU  - Liu, Lihang 
                AU  - Li, Weihua 
                TI  - Lysine-specific histone demethylase 1B (LSD2/KDM1B) represses p53 expression to promote proliferation and inhibit apoptosis in colorectal cancer through LSD2-mediated H3K4me2 demethylation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103558
                DO  - 10.18632/aging.103558
                SP  - 14990
                EP  - 15001
                PY  - 
                AB  - Epigenetic alterations have been reported to play critical roles in the development of colorectal cancer (CRC). However, the biological function of the lysine-specific histone demethylase 1B (LSD2/KDM1B) in CRC is not well understood. Therefore, we investigated the characteristics of LSD2 in CRC. We observed significant upregulation of LSD2 in CRC tissue compared to that in normal colorectal tissue. LSD2 promotes CRC cell proliferation and inhibits cell apoptosis through cell cycle regulation, promoting CRC progression both in vitro and in vivo. We found that LSD2 performs these functions by inhibiting the p53-p21-Rb pathway. Finally, we found that LSD2 directly binds to p53 and represses p53 expression via H3K4me2 demethylation at the p53 promoter. Our results revealed that LSD2 acts as an oncogene by binding and inhibiting p53 activity in CRC. Thus, LSD2 may be a new molecular target for CRC treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Five-lncRNA signature in plasma exosomes serves as diagnostic biomarker for esophageal squamous cell carcinoma

Zichen Jiao, Ao Yu, Weiwei Rong, Xiaofeng He, Ke Zen, Minke Shi, Tao Wang,

https://doi.org/10.18632/aging.103559 pp 15002—15010

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Jiao Z, Yu A, Rong W, He X, Zen K, Shi M, Wang T, . Five-lncRNA signature in plasma exosomes serves as diagnostic biomarker for esophageal squamous cell carcinoma. . 12:15002-15010. https://doi.org/10.18632/aging.103559

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Jiao, Zichen 
                AU  - Yu, Ao 
                AU  - Rong, Weiwei 
                AU  - He, Xiaofeng 
                AU  - Zen, Ke 
                AU  - Shi, Minke 
                AU  - Wang, Tao 
                TI  - Five-lncRNA signature in plasma exosomes serves as diagnostic biomarker for esophageal squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103559
                DO  - 10.18632/aging.103559
                SP  - 15002
                EP  - 15010
                PY  - 
                AB  - Changes in expression of long non-coding RNAs (lncRNAs) in plasma exosomes can be useful for diagnosis of cancer patients. Here, we conducted a four-stage study to identify plasma exosome lncRNAs with diagnostic potential in esophageal squamous cell carcinoma (ESCC). First, plasma exosome lncRNA expression profiles were examined in ESCC patients, esophagitis patients, and healthy controls using RNA sequencing. Differentially expressed plasma exosome lncRNAs from the lncRNA expression profile were then evaluated by qRT-PCR in a large cohort of ESCC patients, esophagitis patients, and healthy controls. Expression levels of the lncRNAs NR_039819, NR_036133, NR_003353, ENST00000442416.1, and ENST00000416100.1 were significantly higher in exosomes from ESCC patients than non-cancer controls. We also confirmed that levels of these five plasma exosome lncRNAs decreased markedly in ESCC patients after surgery. Our results suggest that these five exosome lncRNAs may serve as highly effective, noninvasive biomarkers for ESCC diagnosis.
                ER  -

Click to copy this citation from the text box above or download the citation:

Circular RNA hsa_circ_0076690 acts as a prognostic biomarker in osteoporosis and regulates osteogenic differentiation of hBMSCs via sponging miR-152

Shijie Han, Mingjie Kuang, Chao Sun, Haifeng Wang, Dachuan Wang, Qian Liu,

https://doi.org/10.18632/aging.103560 pp 15011—15020

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Han S, Kuang M, Sun C, Wang H, Wang D, Liu Q, . Circular RNA hsa_circ_0076690 acts as a prognostic biomarker in osteoporosis and regulates osteogenic differentiation of hBMSCs via sponging miR-152. . 12:15011-15020. https://doi.org/10.18632/aging.103560

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Han, Shijie 
                AU  - Kuang, Mingjie 
                AU  - Sun, Chao 
                AU  - Wang, Haifeng 
                AU  - Wang, Dachuan 
                AU  - Liu, Qian 
                TI  - Circular RNA hsa_circ_0076690 acts as a prognostic biomarker in osteoporosis and regulates osteogenic differentiation of hBMSCs via sponging miR-152
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103560
                DO  - 10.18632/aging.103560
                SP  - 15011
                EP  - 15020
                PY  - 
                AB  - Objective: Osteoporosis is the most common skeletal disease world-wide. The aim of this study is to identify potential circRNA biomarkers for osteoporosis diagnosis and treatment, as well as their roles in regulating osteogenic differentiation.
                Results: Hsa_circ_0076690 expression was significantly decreased in osteoporosis patients compared to control and showed an acceptable diagnostic value in clinical samples. Subsequently, hsa_circ_0076690 was identified to act as a sponge of miR-152. The expression of hsa_circ_0076690 was gradually increased during osteogenic differentiation while miR-152 showed a decreased expression trend. Moreover, osteogenic differentiation was promoted by hsa_circ_0076690 over-expression and remain unchanged by miR-152/hsa_circ_0076690 co-overexpression.
                Conclusions: In conclusion, our study revealed that hsa_circ_0076690 may act as a potential diagnostic biomarker for osteoporosis patients and hsa_circ_0076690 could regulate osteogenic differentiation of hBMSCs via sponging miR-152.
                Materials and methods: A total of 114 participants were enrolled in this study with ethics approvals. CircRNAs were identified by means of RNA-sequencing and qRT-PCR experiment. The clinical significance was measured by ROC curve analysis. Target relationship was validated by luciferase reporter assay. The osteogenic-associated biomarkers and ALP activity were detected by western blots.
                ER  -

Click to copy this citation from the text box above or download the citation:

NVD-BM-mediated genetic biosensor triggers accumulation of 7-dehydrocholesterol and inhibits melanoma via Akt1/NF-ĸB signaling

Jia Liu, Lei Cao, Jun-Ze Qu, Ting-Ting Chen, Zi-Jie Su, Yun-Long Hu, Ying Wang, Ming-Dong Yao, Wen-Hai Xiao, Chun Li, Bo Li, Ying-Jin Yuan,

https://doi.org/10.18632/aging.103562 pp 15021—15036

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liu J, Cao L, Qu J, Chen T, Su Z, Hu Y, Wang Y, Yao M, Xiao W, Li C, Li B, Yuan Y, . NVD-BM-mediated genetic biosensor triggers accumulation of 7-dehydrocholesterol and inhibits melanoma via Akt1/NF-ĸB signaling. . 12:15021-15036. https://doi.org/10.18632/aging.103562

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liu, Jia 
                AU  - Cao, Lei 
                AU  - Qu, Jun-Ze 
                AU  - Chen, Ting-Ting 
                AU  - Su, Zi-Jie 
                AU  - Hu, Yun-Long 
                AU  - Wang, Ying 
                AU  - Yao, Ming-Dong 
                AU  - Xiao, Wen-Hai 
                AU  - Li, Chun 
                AU  - Li, Bo 
                AU  - Yuan, Ying-Jin 
                TI  - NVD-BM-mediated genetic biosensor triggers accumulation of 7-dehydrocholesterol and inhibits melanoma via Akt1/NF-ĸB signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103562
                DO  - 10.18632/aging.103562
                SP  - 15021
                EP  - 15036
                PY  - 
                AB  - Aberrant activation of the cholesterol biosynthesis supports tumor cell growth. In recent years, significant progress has been made by targeting rate-limiting enzymes in cholesterol biosynthesis pathways to prevent carcinogenesis. However, precise mechanisms behind cholesterol degradation in cancer cells have not been comprehensively investigated. Here, we report that codon optimization of the orthologous cholesterol 7-desaturase, NVD-BM from Bombyx mori, significantly slowed melanoma cell proliferation and migration, and inhibited cancer cell engraftment in nude mice, by converting cholesterol to toxic 7-dehydrocholesterol. Based on these observations, we established a synthetic genetic circuit to induce melanoma cell regression by sensing tumor specific signals in melanoma cells. The dual-input signals, RELA proto-oncogene (RELA) and signal transducer and activator of transcription 1 (STAT1), activated NVD-BM expression and repressed melanoma cell proliferation and migration. Mechanically, we observed that NVD-BM decreased Akt1-ser473 phosphorylation and inhibited cytoplasmic RELA translocation. Taken together, NVD-BM was identified as a tumor suppressor in malignant melanoma, and we established a dual-input biosensor to promote cancer cell regression, via Akt1/NF-&#x3BA;B signaling. Our results demonstrate the potential therapeutic effects of cholesterol 7-desaturase in melanoma metabolism, and provides insights for genetic circuits targeting 7-dehydrocholesterol accumulation in tumors.
                ER  -

Click to copy this citation from the text box above or download the citation:

2-methylbenzoyl berbamine, a multi-targeted inhibitor, suppresses the growth of human osteosarcoma through disabling NF-κB, ERK and AKT signaling networks

Weixu Li, Yan Li, Wenjia Tian, Xiuguo Han, Jie Zhao, Zengfeng Xin, Hejia Hu, Jun Li, Kai Hang, Rongzhen Xu,

https://doi.org/10.18632/aging.103565 pp 15037—15049

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li W, Li Y, Tian W, Han X, Zhao J, Xin Z, Hu H, Li J, Hang K, Xu R, . 2-methylbenzoyl berbamine, a multi-targeted inhibitor, suppresses the growth of human osteosarcoma through disabling NF-κB, ERK and AKT signaling networks. . 12:15037-15049. https://doi.org/10.18632/aging.103565

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Weixu 
                AU  - Li, Yan 
                AU  - Tian, Wenjia 
                AU  - Han, Xiuguo 
                AU  - Zhao, Jie 
                AU  - Xin, Zengfeng 
                AU  - Hu, Hejia 
                AU  - Li, Jun 
                AU  - Hang, Kai 
                AU  - Xu, Rongzhen 
                TI  - 2-methylbenzoyl berbamine, a multi-targeted inhibitor, suppresses the growth of human osteosarcoma through disabling NF-κB, ERK and AKT signaling networks
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103565
                DO  - 10.18632/aging.103565
                SP  - 15037
                EP  - 15049
                PY  - 
                AB  - Osteosarcoma is the most common malignant bone tumor in children and young adults, and it has a survival rate of only 60% with current cytotoxic chemotherapy combined with aggressive surgery. The aim of this study was to evaluate the therapeutic efficacy of the berbamine derivative 2-methylbenzoyl berbamine (BBD24) for osteosarcoma in vitro and in vivo. We used human osteosarcoma cell lines, primary osteosarcoma cells and mouse models to evaluate the inhibitory effects of BBD24 on osteosarcoma and to determine the molecular mechanism. Our results showed that BBD24 inhibited the growth of the human osteosarcoma cell lines HOS and MG63 in a time- and dose-dependent manner. BBD24 also exhibited significant inhibitory effects on primary osteosarcoma cells. In contrast, BBD24 did not affect normal blood cells under the same conditions. Treatment with BBD24 induced apoptosis, necrosis and autophagy in osteosarcoma cells. Western blot analysis revealed that BBD24 activated the caspase-dependent pathway and downregulated the NF-kB, AKT, and ERK pathways. Finally, BBD24 treatment induced a significant inhibitory effect on the growth of osteosarcoma in nude mice. Our findings indicate that BBD24 is a multitarget inhibitor and may represent a new type of anticancer agent for osteosarcoma treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Establishing a density-based method to separate proliferating and senescent cells from bone marrow stromal cells

Fei Xu, Qiang Zhang, Haitao Wang,

https://doi.org/10.18632/aging.103569 pp 15050—15057

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu F, Zhang Q, Wang H, . Establishing a density-based method to separate proliferating and senescent cells from bone marrow stromal cells. . 12:15050-15057. https://doi.org/10.18632/aging.103569

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xu, Fei 
                AU  - Zhang, Qiang 
                AU  - Wang, Haitao 
                TI  - Establishing a density-based method to separate proliferating and senescent cells from bone marrow stromal cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103569
                DO  - 10.18632/aging.103569
                SP  - 15050
                EP  - 15057
                PY  - 
                AB  - To assist in the study of cellular aging, we established a new method of enriching physiologically aged bone marrow stromal cells (BMSCs) in animals of any age using a Percoll density gradient centrifugation technique. BMSCs from mice 2 months of age were isolated, and their cellular age determined (over 80% Scal-1+ CD29+ CD11b- CD45- CD105- and able to differentiate into osteoblasts, adipocytes, and chondrocytes). As proof &#x2013;of principle, cells were aged in vitro and confirmed by low bromodeoxyuridine (BrdU) incorporation and senescence-associated &#x3B2;-galactosidase (SA-&#x3B2;-gal) staining. Proliferating cells were enriched in high-density gradient layers, and senescent cells were enriched in low-density gradient layers. We confirmed that over 80% of cells from the low-density gradient layer were senescent with SA-&#x3B2;-gal staining and telomere dysfunction-induced foci (TIF) assay. This density-based method, which can separate proliferating and senescent BMSCs, could be used to study mechanisms of physiologic cell aging and may have implications for the use of BMSCs in clinical transplant applications.
                ER  -

Click to copy this citation from the text box above or download the citation:

Cortical atrophy mediates the accumulating effects of vascular risk factors on cognitive decline in the Alzheimer’s disease spectrum

Qing Wang, Cancan He, Yao Zhu, Qianqian Zhang, Zhijun Zhang, Chunming Xie,

https://doi.org/10.18632/aging.103573 pp 15058—15076

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang Q, He C, Zhu Y, Zhang Q, Zhang Z, Xie C, . Cortical atrophy mediates the accumulating effects of vascular risk factors on cognitive decline in the Alzheimer’s disease spectrum. . 12:15058-15076. https://doi.org/10.18632/aging.103573

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Qing 
                AU  - He, Cancan 
                AU  - Zhu, Yao 
                AU  - Zhang, Qianqian 
                AU  - Zhang, Zhijun 
                AU  - Xie, Chunming 
                TI  - Cortical atrophy mediates the accumulating effects of vascular risk factors on cognitive decline in the Alzheimer’s disease spectrum
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103573
                DO  - 10.18632/aging.103573
                SP  - 15058
                EP  - 15076
                PY  - 
                AB  - There are increasing concerns regarding the association of vascular risk factors (VRFs) and cognitive decline in the Alzheimer&apos;s disease (AD) spectrum. Currently, we investigated whether the accumulating effects of VRFs influenced gray matter volumes and subsequently led to cognitive decline in the AD spectrum. Mediation analysis was used to explore the association among VRFs, cortical atrophy, and cognition in the AD spectrum. 123 AD spectrum were recruited and VRF scores were constructed. Multivariate linear regression analysis revealed that higher VRF scores were correlated with lower Mini-Mental State Examination scores and higher Alzheimer&apos;s Disease Assessment Scale-Cognitive Subscale scores, indicating higher VRF scores lead to severer cognitive decline in the AD spectrum. In addition, subjects with higher VRF scores suffered severe cortical atrophy, especially in medial prefrontal cortex and medial temporal lobe. More importantly, common circuits of VRFs- and cognitive decline associated with gray matter atrophy were identified. Further, using mediation analysis, we demonstrated that cortical atrophy regions significantly mediated the relationship between VRF scores and cognitive decline in the AD spectrum. These findings highlight the importance of accumulating risk in the vascular contribution to AD spectrum, and targeting VRFs may provide new strategies for the therapeutic and prevention of AD.
                ER  -

Click to copy this citation from the text box above or download the citation:

Prognostic validation and treatment decision making of the 8^th edition of the American Joint Committee on Cancer pathological staging system for elderly women with early-stage breast cancer

San-Gang Wu, Jian Shi, Wen-Wen Zhang, Jun Wang, Chen-Lu Lian, Jian Lei, Li Hua, Juan Zhou, Zhen-Yu He,

https://doi.org/10.18632/aging.103574 pp 15077—15090

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wu S, Shi J, Zhang W, Wang J, Lian C, Lei J, Hua L, Zhou J, He Z, . Prognostic validation and treatment decision making of the 8^th edition of the American Joint Committee on Cancer pathological staging system for elderly women with early-stage breast cancer. . 12:15077-15090. https://doi.org/10.18632/aging.103574

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Wu, San-Gang 
 AU - Shi, Jian 
 AU - Zhang, Wen-Wen 
 AU - Wang, Jun 
 AU - Lian, Chen-Lu 
 AU - Lei, Jian 
 AU - Hua, Li 
 AU - Zhou, Juan 
 AU - He, Zhen-Yu 
 TI - Prognostic validation and treatment decision making of the 8th edition of the American Joint Committee on Cancer pathological staging system for elderly women with early-stage breast cancer
 JO - 
 JA - 
 VL - 12
 IS - 14
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103574
 DO - 10.18632/aging.103574
 SP - 15077
 EP - 15090
 PY - 
 AB - Purpose: To determine the prognostication and treatment decision making of the American Joint Committee on Cancer (AJCC) 8th pathological staging system in elderly women (aged &#x2265;65 years) with T1-2N0M0 breast cancer (BC).Results: We included 67699 patients, and patients were restaged into stage IA (84.9%), IB (8.9%), and IIA (6.2%) using the 8th AJCC edition criteria. Overall, 69.4% and 30.6% of them underwent breast-conservation surgery (BCS) and mastectomy (MAST), respectively. In patients who received BCS, 30.3% of them underwent postoperative radiotherapy (RT). Patients with a higher pathological stage were more likely to receive MAST. The 5-year breast cancer-specific mortality rate was 2.2%, 6.5% and 13.7% in stage IA, IB, and IIA, respectively. Patients treated with BCS and RT had significantly lower risk of breast cancer-specific mortality compared to those treated with MAST or with BCS alone regardless of the pathological prognostic stages (P&lt;0.001).Conclusions: The 8th AJCC pathological prognostic staging system provides accurate risk stratification and impacts the treatment decision making for elderly women with early-stage BC.Methods: We identified stage T1-2N0M0 BC patients using the Surveillance, Epidemiology, and End Results database. Statistical analyses were used binomial logistic regression, and multivariable competing risk models in the Cox model framework.
 ER -

Click to copy this citation from the text box above or download the citation:

Effects of enriched branched-chain amino acid supplementation on sarcopenia

Chun-Hung Ko, Shin-Jiuan Wu, Shan-Tair Wang, Yin-Fan Chang, Chin-Sung Chang, Ta-Shen Kuan, Hua-Ying Chuang, Chia-Ming Chang, Willy Chou, Chih-Hsing Wu,

https://doi.org/10.18632/aging.103576 pp 15091—15103

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ko C, Wu S, Wang S, Chang Y, Chang C, Kuan T, Chuang H, Chang C, Chou W, Wu C, . Effects of enriched branched-chain amino acid supplementation on sarcopenia. . 12:15091-15103. https://doi.org/10.18632/aging.103576

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ko, Chun-Hung 
                AU  - Wu, Shin-Jiuan 
                AU  - Wang, Shan-Tair 
                AU  - Chang, Yin-Fan 
                AU  - Chang, Chin-Sung 
                AU  - Kuan, Ta-Shen 
                AU  - Chuang, Hua-Ying 
                AU  - Chang, Chia-Ming 
                AU  - Chou, Willy 
                AU  - Wu, Chih-Hsing 
                TI  - Effects of enriched branched-chain amino acid supplementation on sarcopenia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103576
                DO  - 10.18632/aging.103576
                SP  - 15091
                EP  - 15103
                PY  - 
                AB  - To evaluate the effects of short-term administration of enriched branched-chain amino acids (BCAAs) on subjects with pre-sarcopenia or sarcopenia, our quasi-experimental study enrolled 33 subjects (12 pre-sarcopenia/21 sarcopenia; 6 men/27 women; mean age 66.6 &#xB1; 10.3 years) to take one sachet (3.6 g) of enriched BCAA powder twice a day for five weeks followed by a discontinuation period of 12 weeks. We evaluated sarcopenic parameters, including grip strength, 6-meter gait speed, and bioelectrical-impedance-analysis-derived skeletal mass index (SMI), at baseline, 5 weeks, and 17 weeks. We found that both pre-sarcopenic and sarcopenic subjects showed improved SMI, gait speed, and grip strength at 5 weeks. However, all three parameters progressively declined at 17 weeks, especially SMI and grip strength in subjects aged &lt; 65 years and gait speed and grip strength in subjects aged &#x2265; 65 years. It thus appears that supplementation with enriched BCAAs for 5 weeks correlates with short-term positive effects on sarcopenic parameters but attenuation of those effects following discontinuation for 12 weeks.
                ER  -

Click to copy this citation from the text box above or download the citation:

Essential role of STAT5a in DCIS formation and invasion following estrogen treatment

Sundee Dees, Laura Pontiggia, Jean-Francois Jasmin, Federica Sotgia, Michael P. Lisanti, Isabelle Mercier,

https://doi.org/10.18632/aging.103586 pp 15104—15120

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Dees S, Pontiggia L, Jasmin J, Sotgia F, Lisanti MP, Mercier I, . Essential role of STAT5a in DCIS formation and invasion following estrogen treatment. . 12:15104-15120. https://doi.org/10.18632/aging.103586

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Dees, Sundee 
                AU  - Pontiggia, Laura 
                AU  - Jasmin, Jean-Francois 
                AU  - Sotgia, Federica 
                AU  - Lisanti, Michael P. 
                AU  - Mercier, Isabelle 
                TI  - Essential role of STAT5a in DCIS formation and invasion following estrogen treatment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103586
                DO  - 10.18632/aging.103586
                SP  - 15104
                EP  - 15120
                PY  - 
                AB  - Ductal carcinoma in situ (DCIS) is one of the earliest stages of breast cancer (BCa). The mechanisms by which DCIS lesions progress to an invasive state while others remain indolent are yet to be fully characterized and both diagnosis and treatment of this pre-invasive disease could benefit from better understanding the pathways involved. While a decreased expression of Caveolin-1 (Cav-1) in the tumor microenvironment of patients with DCIS breast cancer was linked to progression to invasive breast cancer (IBC), the downstream effector(s) contributing to this process remain elusive. The current report shows elevated expression of Signal Transducer and Activator of Transcription 5a (STAT5a) within the DCIS-like lesions in Cav-1 KO mice following estrogen treatment and inhibition of STAT5a expression prevented the formation of these mammary lesions. In addition, STAT5a overexpression in a human DCIS cell line (MCF10DCIS.com) promoted their invasion, a process accelerated by estrogen treatment and associated with increased levels of the matrix metalloproteinase-9 (MMP-9) precursor. In sum, our results demonstrate a novel regulatory axis (Cav-1&#x2666;STAT5a&#x2666;MMP-9) in DCIS that is fully activated by the presence of estrogen. Our sudies suggest to further study phosphorylated STAT5a (Y694) as a potential biomarker to guide and predict outcome of DCIS patient population.
                ER  -

Click to copy this citation from the text box above or download the citation:

Megakaryocytes promote osteoclastogenesis in aging

Deepa Kanagasabapathy, Rachel J. Blosser, Kevin A. Maupin, Jung Min Hong, Marta Alvarez, Joydeep Ghosh, Safa F. Mohamad, Alexandra Aguilar-Perez, Edward F. Srour, Melissa A. Kacena, Angela Bruzzaniti,

https://doi.org/10.18632/aging.103595 pp 15121—15133

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Kanagasabapathy D, Blosser RJ, Maupin KA, Hong JM, Alvarez M, Ghosh J, Mohamad SF, Aguilar-Perez A, Srour EF, Kacena MA, Bruzzaniti A, . Megakaryocytes promote osteoclastogenesis in aging. . 12:15121-15133. https://doi.org/10.18632/aging.103595

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Kanagasabapathy, Deepa 
                AU  - Blosser, Rachel J. 
                AU  - Maupin, Kevin A. 
                AU  - Hong, Jung Min 
                AU  - Alvarez, Marta 
                AU  - Ghosh, Joydeep 
                AU  - Mohamad, Safa F. 
                AU  - Aguilar-Perez, Alexandra 
                AU  - Srour, Edward F. 
                AU  - Kacena, Melissa A. 
                AU  - Bruzzaniti, Angela 
                TI  - Megakaryocytes promote osteoclastogenesis in aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103595
                DO  - 10.18632/aging.103595
                SP  - 15121
                EP  - 15133
                PY  - 
                AB  - Megakaryocytes (MKs) support bone formation by stimulating osteoblasts (OBs) and inhibiting osteoclasts (OCs). Aging results in higher bone resorption, leading to bone loss. Whereas previous studies showed the effects of aging on MK-mediated bone formation, the effects of aging on MK-mediated OC formation is poorly understood. Here we examined the effect of thrombopoietin (TPO) and MK-derived conditioned media (CM) from young (3-4 months) and aged (22-25 months) mice on OC precursors. Our findings showed that aging significantly increased OC formation in vitro. Moreover, the expression of the TPO receptor, Mpl, and circulating TPO levels were elevated in the bone marrow cavity. We previously showed that MKs from young mice secrete factors that inhibit OC differentiation. However, rather than inhibiting OC development, we found that MKs from aged mice promote OC formation. Interestingly, these age-related changes in MK functionality were only observed using female MKs, potentially implicating the sex steroid, estrogen, in signaling. Further, RANKL expression was highly elevated in aged MKs suggesting MK-derived RANKL signaling may promote osteoclastogenesis in aging. Taken together, these data suggest that modulation in TPO-Mpl expression in bone marrow and age-related changes in the MK secretome promote osteoclastogenesis to impact skeletal aging.
                ER  -

Click to copy this citation from the text box above or download the citation:

Signatures of cell stress and altered bioenergetics in skin fibroblasts from patients with multiple sclerosis

Jordan M. Wilkins, Oleksandr Gakh, Parijat Kabiraj, Christina B. McCarthy, W. Oliver Tobin, Charles L. Howe, Claudia F. Lucchinetti,

https://doi.org/10.18632/aging.103612 pp 15134—15156

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wilkins JM, Gakh O, Kabiraj P, McCarthy CB, Tobin WO, Howe CL, Lucchinetti CF, . Signatures of cell stress and altered bioenergetics in skin fibroblasts from patients with multiple sclerosis. . 12:15134-15156. https://doi.org/10.18632/aging.103612

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wilkins, Jordan M. 
                AU  - Gakh, Oleksandr 
                AU  - Kabiraj, Parijat 
                AU  - McCarthy, Christina B. 
                AU  - Tobin, W. Oliver 
                AU  - Howe, Charles L. 
                AU  - Lucchinetti, Claudia F. 
                TI  - Signatures of cell stress and altered bioenergetics in skin fibroblasts from patients with multiple sclerosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103612
                DO  - 10.18632/aging.103612
                SP  - 15134
                EP  - 15156
                PY  - 
                AB  - Multiple sclerosis (MS) is a central nervous system inflammatory demyelinating disease and the most common cause of non-traumatic disability in young adults. Despite progress in the treatment of the active relapsing disease, therapeutic options targeting irreversible progressive decline remain limited. Studies using skin fibroblasts derived from patients with neurodegenerative disorders demonstrate that cell stress pathways and bioenergetics are altered when compared to healthy individuals. However, findings in MS skin fibroblasts are limited. Here, we collected skin fibroblasts from 24 healthy control individuals, 30 patients with MS, and ten with amyotrophic lateral sclerosis (ALS) to investigate altered cell stress profiles. We observed endoplasmic reticulum swelling in MS skin fibroblasts, and increased gene expression of cell stress markers including BIP, ATF4, CHOP, GRP94, P53, and P21. When challenged against hydrogen peroxide, MS skin fibroblasts had reduced resiliency compared to ALS and controls. Mitochondrial and glycolytic functions were perturbed in MS skin fibroblasts while exhibiting a significant increase in lactate production over ALS and controls. Our results suggest that MS skin fibroblasts have an underlying stress phenotype, which may be disease specific. Interrogating MS skin fibroblasts may provide patient specific molecular insights and aid in prognosis, diagnosis, and therapeutic testing enhancing individualized medicine.
                ER  -

Click to copy this citation from the text box above or download the citation:

Physical robustness and resilience among long-lived female siblings: a comparison with sporadic long-livers

Angéline Galvin, Svetlana Ukraintseva, Konstantin Arbeev, Mary Feitosa, Kaare Christensen,

https://doi.org/10.18632/aging.103618 pp 15157—15168

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Galvin A, Ukraintseva S, Arbeev K, Feitosa M, Christensen K, . Physical robustness and resilience among long-lived female siblings: a comparison with sporadic long-livers. . 12:15157-15168. https://doi.org/10.18632/aging.103618

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Galvin, Angéline 
                AU  - Ukraintseva, Svetlana 
                AU  - Arbeev, Konstantin 
                AU  - Feitosa, Mary 
                AU  - Christensen, Kaare 
                TI  - Physical robustness and resilience among long-lived female siblings: a comparison with sporadic long-livers
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103618
                DO  - 10.18632/aging.103618
                SP  - 15157
                EP  - 15168
                PY  - 
                AB  - Long-lived individuals are central in studies of healthy longevity. However, few pro-longevity factors have been identified, presumably because of &#x201C;phenocopies&#x201D;, i.e. individuals that live long by chance. Familial longevity cases may include less phenocopies than sporadic cases and provide better insights into longevity mechanisms. Here we examined whether long-lived female siblings have a better ability to avoid diseases at ages 65+ (proxy for &#x201C;robustness&#x201D;) and/or survive to extreme ages (proxy for &#x201C;resilience&#x201D;) compared to sporadic long-livers. A total of 1,156 long-lived female siblings were selected from three nationwide Danish studies and age-matched with sporadic long-lived female controls. Outcomes included cumulative incidence of common health disorders from age 65 and overall survival. Long-lived female siblings had lower risks of some but not all health conditions, most significantly, depression (OR=0.74; 95%CI=0.62-0.88), and less significantly hypertensive (OR=0.84; 95%CI=0.71-0.99) and cerebrovascular (OR=0.73; 95%CI=0.55-0.96) diseases. They also had consistently better survival to extreme ages (HR=0.71; 95%CI= 0.63-0.81) compared to sporadic long-livers. After adjustment for the diseases, the association with mortality changed only marginally suggesting central role of better physiological resilience in familial longevity. Due to their consistently better resilience, familial longevity cases could be more informative than sporadic cases for studying mechanisms of healthy longevity.
                ER  -

Click to copy this citation from the text box above or download the citation:

Role of CPEB3 protein in learning and memory: new insights from synaptic plasticity

Wen Rui Qu, Qi Han Sun, Qian Qian Liu, Hong Juan Jin, Ran Ji Cui, Wei Yang, De Biao Song, Bing Jin Li,

https://doi.org/10.18632/aging.103404 pp 15169—15182

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Qu WR, Sun QH, Liu QQ, Jin HJ, Cui RJ, Yang W, Song DB, Li BJ, . Role of CPEB3 protein in learning and memory: new insights from synaptic plasticity. . 12:15169-15182. https://doi.org/10.18632/aging.103404

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Qu, Wen Rui 
                AU  - Sun, Qi Han 
                AU  - Liu, Qian Qian 
                AU  - Jin, Hong Juan 
                AU  - Cui, Ran Ji 
                AU  - Yang, Wei 
                AU  - Song, De Biao 
                AU  - Li, Bing Jin 
                TI  - Role of CPEB3 protein in learning and memory: new insights from synaptic plasticity
                JO  - 
                JA  - 
                VL  - 12
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103404
                DO  - 10.18632/aging.103404
                SP  - 15169
                EP  - 15182
                PY  - 
                AB  - The cytoplasmic polyadenylation element-binding (CPEB) protein family have demonstrated a crucial role for establishing synaptic plasticity and memory in model organisms. In this review, we outline evidence for CPEB3 as a crucial regulator of learning and memory, citing evidence from behavioral, electrophysiological and morphological studies. Subsequently, the regulatory role of CPEB3 is addressed in the context of the plasticity-related proteins, including AMPA and NMDA receptor subunits, actin, and the synaptic scaffolding protein PSD95. Finally, we delve into some of the more well-studied molecular mechanisms that guide the functionality of this dynamic regulator both during synaptic stimulation and in its basal state, including a variety of upstream regulators, post-translational modifications, and important structural domains that confer the unique properties of CPEB3. Collectively, this review offers a comprehensive view of the regulatory layers that allow a pathway for CPEB3&#x2019;s maintenance of translational control that guides the necessary protein changes required for the establishment and maintenance of lasting synaptic plasticity and ultimately, long term learning and memory.
                ER  -

Click to copy this citation from the text box above or download the citation:

Correction for: TRIM29 mediates lung squamous cell carcinoma cell metastasis by regulating autophagic degradation of E-cadherin

Weifeng Xu, Beibei Chen, Dianshan Ke, Xiaobing Chen,

https://doi.org/10.18632/aging.103873 pp 15183

PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu W, Chen B, Ke D, Chen X, . Correction for: TRIM29 mediates lung squamous cell carcinoma cell metastasis by regulating autophagic degradation of E-cadherin. . 12:15183-15183. https://doi.org/10.18632/aging.103873

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

Volume 12, Issue 14

About the Cover

Editorials

Qiyu Tian, Xiangdong Liu, Min Du,

Cite this Article

How to cite

Copy or Download citation:

Candice E. Van Skike, Veronica Galvan,

Cite this Article

How to cite

Copy or Download citation:

Research Papers

COVID-19 High neutrophil-to-lymphocyte ratio associated with progression to critical illness in older patients with COVID-19: a multicenter retrospective study

Jiangshan Lian, Ciliang jin, Shaorui Hao, Xiaoli Zhang, Meifang Yang, Xi Jin, Yingfeng Lu, Jianhua Hu, Shanyan Zhang, Lin Zheng, Hongyu Jia, Huan Cai, Yimin Zhang, Guodong Yu, Xiaoyan Wang, Jueqing Gu, Chanyuan Ye, Xiaopeng Yu, Jianguo Gao, Yida Yang, Jifang Sheng,

Cite this Article

How to cite

Copy or Download citation:

COVID-19 Clinical imaging characteristics of inpatients with coronavirus disease-2019 in Heilongjiang Province, China: a retrospective study

Hao Jiang, Wei Guo, Zhongxing Shi, Huijie Jiang, Mingyu Zhang, Lai Wei, Yongmei Pan,

Cite this Article

How to cite

Copy or Download citation:

COVID-19 Risk of death by age and gender from CoVID-19 in Peru, March-May, 2020

Cesar Munayco, Gerardo Chowell, Amna Tariq, Eduardo A. Undurraga, Kenji Mizumoto,

Cite this Article

How to cite

Copy or Download citation:

COVID-19 Development and validation of a risk stratification model for screening suspected cases of COVID-19 in China

Jing Ma, Xiaowei Shi, Weiming Xu, Feifei Lv, Jian Wu, Qiaoling Pan, Jinfeng Yang, Jiong Yu, Hongcui Cao, Lanjuan Li,

Cite this Article

How to cite

Copy or Download citation:

COVID-19 COVID-19 induced liver function abnormality associates with age

Shasha Li, Jinsong Li, Zhenhua Zhang, Lin Tan, Tuo Shao, Ming Li, Xiuyong Li, Jacinta A. Holmes, Wenyu Lin, Mingfeng Han,

Cite this Article

How to cite

Copy or Download citation:

Sara Romero-Vázquez, Alfredo Adán, Marc Figueras-Roca, Victor Llorenç, Mark Slevin, Gemma Vilahur, Lina Badimon, Andrew D Dick, Blanca Molins,

Cite this Article

How to cite

Copy or Download citation:

Anna Lewinska, Jagoda Adamczyk-Grochala, Dominika Bloniarz, Beata Horeczy, Slawomir Zurek, Arkadiusz Kurowicki, Bogumila Woloszczuk-Gebicka, Kazimierz Widenka, Maciej Wnuk,

Cite this Article

How to cite

Copy or Download citation:

Cite this Article

How to cite

Copy or Download citation:

Brijesh Kumar Singh, Madhulika Tripathi, Reddemma Sandireddy, Keziah Tikno, Jin Zhou, Paul Michael Yen,

Cite this Article

How to cite

Copy or Download citation:

Marco Raffaele, Kristina Kovacovicova, Francesca Bonomini, Rita Rezzani, Jan Frohlich, Manlio Vinciguerra,

Cite this Article

How to cite

Copy or Download citation:

Lan Xiang, Qiaobei Wu, Hiroyuki Osada, Minoru Yoshida, Wensheng Pan, Jianhua Qi,

Cite this Article

How to cite

Copy or Download citation:

Yalan Zhao, Xiaobo Zhou, Xue Zhao, Xinyang Yu, Andi Wang, Xuyang Chen, Hongbo Qi, Ting-Li Han, Hua Zhang, Philip N. Baker,

Cite this Article

How to cite

Copy or Download citation:

Fei Dai, Fei Luo, Rui Zhou, Qiang Zhou, Jianzhong Xu, Zehua Zhang, Jun Xiao, Lei Song,

Cite this Article

How to cite

Copy or Download citation:

Wenjin Guo, Juxiong Liu, Yufei Zhang, He Ma, Yuhang Li, Qian Gong, Yu Cao, Guiqiu Hu, Shengnan Xie, Shoupeng Fu,

Cite this Article

How to cite

Copy or Download citation:

Yun Yu, Kaipeng Xie, Qinglin Lou, Hui Xia, Dan Wu, Lingli Dai, Cuining Hu, Kunlin Wang, Shan Shan, Yun Hu, Wei Tang,

Cite this Article

How to cite

Copy or Download citation:

Jing Zhou, Ze-Ning Dong, Bai-Quan Qiu, Ming Hu, Xiao-Qing Liang, Xing Dai, Dan Hong, Yu-Fang Sun,

Cite this Article

How to cite

Copy or Download citation:

COVID-19
High neutrophil-to-lymphocyte ratio associated with progression to critical illness in older patients with COVID-19: a multicenter retrospective study

COVID-19
Clinical imaging characteristics of inpatients with coronavirus disease-2019 in Heilongjiang Province, China: a retrospective study

COVID-19
Risk of death by age and gender from CoVID-19 in Peru, March-May, 2020

COVID-19
Development and validation of a risk stratification model for screening suspected cases of COVID-19 in China

COVID-19
COVID-19 induced liver function abnormality associates with age