Volume 12, Issue 22

Criddle RS, Lin HL, James I, Park JS, Hansen LD, Price JC, . Proposing a minimal set of metrics and methods to predict probabilities of amyloidosis disease and onset age in individuals. . 12:22356-22369. https://doi.org/10.18632/aging.202208

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                TY  - JOUR
                AU  - Criddle, Richard S. 
                AU  - Lin, Hsien-Jung L. 
                AU  - James, Isabella 
                AU  - Park, Ji Sun 
                AU  - Hansen, Lee D. 
                AU  - Price, John C. 
                TI  - Proposing a minimal set of metrics and methods to predict probabilities of amyloidosis disease and onset age in individuals
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202208
                DO  - 10.18632/aging.202208
                SP  - 22356
                EP  - 22369
                PY  - 
                AB  - Many amyloid-driven pathologies have both genetic and stochastic components where assessing risk of disease development requires a multifactorial assessment where many of the variables are poorly understood. Risk of transthyretin-mediated amyloidosis is enhanced by age and mutation of the transthyretin (TTR) gene, but amyloidosis is not directly initiated by mutated TTR proteins. Nearly all of the 150+ known mutations increase dissociation of the homotetrameric protein structure and increase the probability of an individual developing a TTR amyloid disease late in life. TTR amyloidosis is caused by dissociated monomers that are destabilized and refold into an amyloidogenic form. Therefore, monomer concentration, monomer proteolysis rate, and structural stability are key variables that may determine the rate of development of amyloidosis. Here we develop a unifying biophysical model that quantifies the relationships among these variables in plasma and suggest the probability of an individual developing a TTR amyloid disease can be estimated. This may allow quantification of risk for amyloidosis and provide the information necessary for development of methods for early diagnosis and prevention. Given the similar observation of genetic and sporadic amyloidoses for other diseases, this model and the measurements to assess risk may be applicable to more proteins than just TTR.
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COVID-19
Genomic, epigenomic, and immune subtype analysis of CTSL/B and SARS-CoV-2 receptor ACE2 in pan-cancer

Huimin Li, Longxiang Xie, Lin Chen, Lu Zhang, Yali Han, Zhongyi Yan, Xiangqian Guo,

https://doi.org/10.18632/aging.104147 pp 22370—22389

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Li H, Xie L, Chen L, Zhang L, Han Y, Yan Z, Guo X, . Genomic, epigenomic, and immune subtype analysis of CTSL/B and SARS-CoV-2 receptor ACE2 in pan-cancer. . 12:22370-22389. https://doi.org/10.18632/aging.104147

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                TY  - JOUR
                AU  - Li, Huimin 
                AU  - Xie, Longxiang 
                AU  - Chen, Lin 
                AU  - Zhang, Lu 
                AU  - Han, Yali 
                AU  - Yan, Zhongyi 
                AU  - Guo, Xiangqian 
                TI  - Genomic, epigenomic, and immune subtype analysis of CTSL/B and SARS-CoV-2 receptor ACE2 in pan-cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104147
                DO  - 10.18632/aging.104147
                SP  - 22370
                EP  - 22389
                PY  - 
                AB  - SARS-coronavirus 2 (SARS-CoV-2) has been spreading widely and posing an international challenge for both healthcare and society. At present, cancer has been identified as an individual risk factor for COVID-19. Angiotensin converting enzyme 2 (ACE2) and Cathepsin L/Cathepsin B (CTSL/B), which act as the receptor and entry-associated proteases of SARS-CoV-2 respectively, are pivotal for SARS-CoV-2 infection. To investigate the possible SARS-CoV-2 infection risk of pan-cancer, we analyzed the genetic alterations, RNA expression, DNA methylation, and the association with immune subtypes of ACE2 and CTSL/B with the prognosis in pan-cancer. Results showed the upregulation of CTSL/B and ACE2 in Pancreatic adenocarcinoma (PAAD) and Stomach adenocarcinoma (STAD) and demonstrated a positive correlation between copy number alteration (CNA) and gene expression for CTSB in PAAD and STAD. Hypomethylation and a negative correlation of gene expression and methylation for CTSB were detected in PAAD. In addition, ACE2 and CTSL/B are overexpressed in the IFN-gamma immune subtype of ovarian serous Cystadenocarcinoma (OV), Cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), and Bladder urothelial carcinoma (BLCA). Our study presents a bioinformatics assessment for the potential risk of SARS-CoV-2 infection in pan-cancer.
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COVID-19
High incidence of stroke in COVID-19 patients

Jingyu Chen, Yazhou Wu, Zhi Chen, Bin Yi, Lili Zhang, Changlin Yin, Hua Feng,

https://doi.org/10.18632/aging.104092 pp 22390—22398

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Chen J, Wu Y, Chen Z, Yi B, Zhang L, Yin C, Feng H, . High incidence of stroke in COVID-19 patients. . 12:22390-22398. https://doi.org/10.18632/aging.104092

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                TY  - JOUR
                AU  - Chen, Jingyu 
                AU  - Wu, Yazhou 
                AU  - Chen, Zhi 
                AU  - Yi, Bin 
                AU  - Zhang, Lili 
                AU  - Yin, Changlin 
                AU  - Feng, Hua 
                TI  - High incidence of stroke in COVID-19 patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104092
                DO  - 10.18632/aging.104092
                SP  - 22390
                EP  - 22398
                PY  - 
                AB  - A retrospective analysis of 11 COVID-19 patients complicated with stroke was performed. It was found that the incidence of stroke in patients with COVID-19 was significantly higher than the average level of the general population (P=0.003), and the D-dimer levels of 11 stroke patients were significantly higher than other patients (P=0.004). The significant increase of D-dimer can be used as an early warning indicator of cerebral infarction. It is critical to have a response plan for treating acute stroke in COVID-19 patients.
                ER  -

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COVID-19
Impact of age on duration of viral RNA shedding in patients with COVID-19

Chenliang Zhou, Tianfang Zhang, Haotang Ren, Shanshan Sun, Xia Yu, Jifang Sheng, Yu Shi, Hong Zhao,

https://doi.org/10.18632/aging.104114 pp 22399—22404

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Zhou C, Zhang T, Ren H, Sun S, Yu X, Sheng J, Shi Y, Zhao H, . Impact of age on duration of viral RNA shedding in patients with COVID-19. . 12:22399-22404. https://doi.org/10.18632/aging.104114

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                TY  - JOUR
                AU  - Zhou, Chenliang 
                AU  - Zhang, Tianfang 
                AU  - Ren, Haotang 
                AU  - Sun, Shanshan 
                AU  - Yu, Xia 
                AU  - Sheng, Jifang 
                AU  - Shi, Yu 
                AU  - Zhao, Hong 
                TI  - Impact of age on duration of viral RNA shedding in patients with COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104114
                DO  - 10.18632/aging.104114
                SP  - 22399
                EP  - 22404
                PY  - 
                AB  - Background: The aim of this study was to investigate the host factors of patients with COVID-19 that were associated with delayed viral RNA clearance in specimens obtained from the upper respiratory tract.
                Results: A median of a 32-day period of viral RNA shedding was observed, ranging from 4 days to 111 days. On multivariate analysis, elderly age was independently associated with prolonged viral shedding (OR = 1.02, 95% CI: 1.01&#x2013;1.04, P = 0.003). An incremental increase in the duration of viral RNA shedding was observed with increasing age (P &lt; 0.05). The median (quartile) duration of viral RNA shedding was 23 (22) days (&#x2264; 40 years), 30 (18) days (41&#x2013;50 years), 33 (21) days (51&#x2013;60 years), 34 (17) days (61&#x2013;70 years) and 34 (17) days (&gt; 70 years).
                Conclusions: Viral RNA shedding can persist for as long as 111 days in the upper respiratory tract. Increasing age is associated with viral RNA persistence.
                Method: The demographic and virological data of patients with laboratory-confirmed COVID-19 were retrospectively analyzed. A multivariate logistic regression analysis was performed to identify significant risk factors associated with delayed viral RNA clearance. The duration of viral shedding was compared among age-stratified groups.
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COVID-19
Clinical characteristics of the first known cases of death caused by COVID-19 pneumonia

Fan-Zhen Kong, Yi Wang, Mei-Xia Wang, Qing-Zhang Cheng, Robert Logan, Guan-Hui Wu, Si-Ming Hu,

https://doi.org/10.18632/aging.104171 pp 22405—22412

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Kong F, Wang Y, Wang M, Cheng Q, Logan R, Wu G, Hu S, . Clinical characteristics of the first known cases of death caused by COVID-19 pneumonia. . 12:22405-22412. https://doi.org/10.18632/aging.104171

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                TY  - JOUR
                AU  - Kong, Fan-Zhen 
                AU  - Wang, Yi 
                AU  - Wang, Mei-Xia 
                AU  - Cheng, Qing-Zhang 
                AU  - Logan, Robert 
                AU  - Wu, Guan-Hui 
                AU  - Hu, Si-Ming 
                TI  - Clinical characteristics of the first known cases of death caused by COVID-19 pneumonia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104171
                DO  - 10.18632/aging.104171
                SP  - 22405
                EP  - 22412
                PY  - 
                AB  - Severe pneumonia caused by COVID-19 has resulted in many deaths worldwide. Here, we analyzed the clinical characteristics of the first 17 reported cases of death due to COVID-19 pneumonia in Wuhan, China. Demographics, initial symptoms, complications, chest computerized tomography (CT) images, treatments, and prognoses were collected and analyzed from the National Health Committee of China data. The first 17 reported deaths from COVID-19 were predominately in older men; 82.35% of patients were older than 65 years, and 76.47% were males. The most common initial symptoms were fever or fatigue (14 cases, 82.35%), respiratory symptoms, such as cough (12 cases, 70.59%), and neurological symptoms, such as headache (3 cases, 17.65%). The most common finding of chest CT was viral pneumonia (5 cases, 29.41%). Anti-infectives (11 cases, 64.71%) and mechanical ventilation (9 cases, 52.94%) were commonly used for treatment. Most of the patients (16 cases, 94.12%) died of acute respiratory distress syndrome (ARDS). Our findings show that advanced age and male gender are effective predictors of COVID-19 mortality, and suggest that early interventions to reduce the incidence of ARDS may improve prognosis of COVID-19 pneumonia patients.
                ER  -

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COVID-19
Estimating the release of inflammatory factors and use of glucocorticoid therapy for COVID-19 patients with comorbidities

Dan Han, Chunfen Peng, Rui Meng, Jing Yao, Qiong Zhou, Yong Xiao, Hong Ma,

https://doi.org/10.18632/aging.202172 pp 22413—22424

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Han D, Peng C, Meng R, Yao J, Zhou Q, Xiao Y, Ma H, . Estimating the release of inflammatory factors and use of glucocorticoid therapy for COVID-19 patients with comorbidities. . 12:22413-22424. https://doi.org/10.18632/aging.202172

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                TY  - JOUR
                AU  - Han, Dan 
                AU  - Peng, Chunfen 
                AU  - Meng, Rui 
                AU  - Yao, Jing 
                AU  - Zhou, Qiong 
                AU  - Xiao, Yong 
                AU  - Ma, Hong 
                TI  - Estimating the release of inflammatory factors and use of glucocorticoid therapy for COVID-19 patients with comorbidities
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202172
                DO  - 10.18632/aging.202172
                SP  - 22413
                EP  - 22424
                PY  - 
                AB  - COVID-19 exhibits both variability and rapid progression, particularly in patients with comorbidities such as diabetes, hypertension or cancer. To determine how these underlying disorders exacerbate pneumonia in COVID-19, we evaluated 79 patients with severe COVID-19 and grouped them according to whether or not they had comorbidities. Clinical information, laboratory examinations, immunological function, and treatment outcomes were retrospectively analyzed. Our study revealed that severe COVID-19 patients with comorbidities had higher levels of inflammatory indices, including blood interferon-&#x3B3;, interleukin (IL)-6 and c-reactive protein levels as well as the erythrocyte sedimentation rate. These were accompanied by lymphopenia, hypokalemia, hypoalbuminemia, a decrease in either CD4+ T cells or lymphocyte count, and coagulation disorders, which were closely related to poor prognosis. Patients with comorbidities also had longer disease remission times (27 &#xB1; 6.7 days) than those without comorbidities (20 &#xB1; 6.5 days). Cox multivariate analysis indicated that glucocorticoid therapy and IL-6 were independent prognostic factors. Our findings suggest that coexisting comorbidities aggravate COVID-19 through the excessive release of inflammatory factors and that glucocorticoid therapy may be beneficial.
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COVID-19
In search of preventive strategies: novel high-CBD Cannabis sativa extracts modulate ACE2 expression in COVID-19 gateway tissues

Bo Wang, Anna Kovalchuk, Dongping Li, Rocio Rodriguez-Juarez, Yaroslav Ilnytskyy, Igor Kovalchuk, Olga Kovalchuk,

https://doi.org/10.18632/aging.202225 pp 22425—22444

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Wang B, Kovalchuk A, Li D, Rodriguez-Juarez R, Ilnytskyy Y, Kovalchuk I, Kovalchuk O, . In search of preventive strategies: novel high-CBD Cannabis sativa extracts modulate ACE2 expression in COVID-19 gateway tissues. . 12:22425-22444. https://doi.org/10.18632/aging.202225

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Provider: 
 TY - JOUR
 AU - Wang, Bo 
 AU - Kovalchuk, Anna 
 AU - Li, Dongping 
 AU - Rodriguez-Juarez, Rocio 
 AU - Ilnytskyy, Yaroslav 
 AU - Kovalchuk, Igor 
 AU - Kovalchuk, Olga 
 TI - In search of preventive strategies: novel high-CBD Cannabis sativa extracts modulate ACE2 expression in COVID-19 gateway tissues
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.202225
 DO - 10.18632/aging.202225
 SP - 22425
 EP - 22444
 PY - 
 AB - With the current COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there is an urgent need for new therapies and prevention strategies that can help curtail disease spread and reduce mortality. The inhibition of viral entry and thus spread is a plausible therapeutic avenue.
 SARS-CoV-2 uses receptor-mediated entry into a human host via the angiotensin-converting enzyme 2 (ACE2), which is expressed in lung tissue as well as the oral and nasal mucosa, kidney, testes and gastrointestinal tract. The modulation of ACE2 levels in these gateway tissues may be an effective strategy for decreasing disease susceptibility.
 Cannabis sativa, especially those high in the anti-inflammatory cannabinoid cannabidiol (CBD), has been found to alter gene expression and inflammation and harbour anti-cancer and anti-inflammatory properties. However, its effects on ACE2 expression remain unknown.
 Working under a Health Canada research license, we developed over 800 new C. sativa cultivars and hypothesized that high-CBD C. sativa extracts may be used to down-regulate ACE2 expression in target COVID-19 tissues. Using artificial 3D human models of oral, airway and intestinal tissues, we identified 13 high-CBD C. sativa extracts that decrease ACE2 protein levels. Some C. sativa extracts down-regulate serine protease TMPRSS2, another critical protein required for SARS-CoV-2 entry into host cells.
 While our most effective extracts require further large-scale validation, our study is important for future analyses of the effects of medical cannabis on COVID-19. The extracts of our most successful novel high-CBD C. sativa lines, pending further investigation, may become a useful and safe addition to the prevention/treatment of COVID-19 as an adjunct therapy.
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Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial

Yafit Hachmo, Amir Hadanny, Ramzia Abu Hamed, Malka Daniel-Kotovsky, Merav Catalogna, Gregory Fishlev, Erez Lang, Nir Polak, Keren Doenyas, Mony Friedman, Yonatan Zemel, Yair Bechor, Shai Efrati,

https://doi.org/10.18632/aging.202188 pp 22445—22456

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Hachmo Y, Hadanny A, Abu Hamed R, Daniel-Kotovsky M, Catalogna M, Fishlev G, Lang E, Polak N, Doenyas K, Friedman M, Zemel Y, Bechor Y, Efrati S, . Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial. . 12:22445-22456. https://doi.org/10.18632/aging.202188

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                TY  - JOUR
                AU  - Hachmo, Yafit 
                AU  - Hadanny, Amir 
                AU  - Abu Hamed, Ramzia 
                AU  - Daniel-Kotovsky, Malka 
                AU  - Catalogna, Merav 
                AU  - Fishlev, Gregory 
                AU  - Lang, Erez 
                AU  - Polak, Nir 
                AU  - Doenyas, Keren 
                AU  - Friedman, Mony 
                AU  - Zemel, Yonatan 
                AU  - Bechor, Yair 
                AU  - Efrati, Shai 
                TI  - Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202188
                DO  - 10.18632/aging.202188
                SP  - 22445
                EP  - 22456
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Hachmo, Yafit 
                AU  - Hadanny, Amir 
                AU  - Abu Hamed, Ramzia 
                AU  - Daniel-Kotovsky, Malka 
                AU  - Catalogna, Merav 
                AU  - Fishlev, Gregory 
                AU  - Lang, Erez 
                AU  - Polak, Nir 
                AU  - Doenyas, Keren 
                AU  - Friedman, Mony 
                AU  - Zemel, Yonatan 
                AU  - Bechor, Yair 
                AU  - Efrati, Shai 
                TI  - Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202188
                DO  - 10.18632/aging.202188
                SP  - 22445
                EP  - 22456
                PY  - 
                AB  - Introduction: Aging is characterized by the progressive loss of physiological capacity. At the cellular level, two key hallmarks of the aging process include telomere length (TL) shortening and cellular senescence. Repeated intermittent hyperoxic exposures, using certain hyperbaric oxygen therapy (HBOT) protocols, can induce regenerative effects which normally occur during hypoxia. The aim of the current study was to evaluate whether HBOT affects TL and senescent cell concentrations in a normal, non-pathological, aging adult population.
                Methods: Thirty-five healthy independently living adults, aged 64 and older, were enrolled to receive 60 daily HBOT exposures. Whole blood samples were collected at baseline, at the 30th and 60th session, and 1-2 weeks following the last HBOT session. Peripheral blood mononuclear cells (PBMCs) telomeres length and senescence were assessed.
                Results: Telomeres length of T helper, T cytotoxic, natural killer and B cells increased significantly by over 20% following HBOT. The most significant change was noticed in B cells which increased at the 30th session, 60th session and post HBOT by 25.68%&#xB1;40.42 (p=0.007), 29.39%&#xB1;23.39 (p=0.0001) and 37.63%&#xB1;52.73 (p=0.007), respectively.
                There was a significant decrease in the number of senescent T helpers by -37.30%&#xB1;33.04 post-HBOT (P&lt;0.0001). T-cytotoxic senescent cell percentages decreased significantly by -10.96%&#xB1;12.59 (p=0.0004) post-HBOT.
                In conclusion, the study indicates that HBOT may induce significant senolytic effects including significantly increasing telomere length and clearance of senescent cells in the aging populations.
                ER  -

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Generalized correlation coefficient for genome-wide association analysis of cognitive ability in twins

Afsaneh Mohammadnejad, Marianne Nygaard, Shuxia Li, Dongfeng Zhang, Chunsheng Xu, Weilong Li, Jesper Lund, Lene Christiansen, Jan Baumbach, Kaare Christensen, Jacob v. B. Hjelmborg, Qihua Tan,

https://doi.org/10.18632/aging.104198 pp 22457—22494

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Mohammadnejad A, Nygaard M, Li S, Zhang D, Xu C, Li W, Lund J, Christiansen L, Baumbach J, Christensen K, Hjelmborg JvB, Tan Q, . Generalized correlation coefficient for genome-wide association analysis of cognitive ability in twins. . 12:22457-22494. https://doi.org/10.18632/aging.104198

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                TY  - JOUR
                AU  - Mohammadnejad, Afsaneh 
                AU  - Nygaard, Marianne 
                AU  - Li, Shuxia 
                AU  - Zhang, Dongfeng 
                AU  - Xu, Chunsheng 
                AU  - Li, Weilong 
                AU  - Lund, Jesper 
                AU  - Christiansen, Lene 
                AU  - Baumbach, Jan 
                AU  - Christensen, Kaare 
                AU  - Hjelmborg, Jacob v. B. 
                AU  - Tan, Qihua 
                TI  - Generalized correlation coefficient for genome-wide association analysis of cognitive ability in twins
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104198
                DO  - 10.18632/aging.104198
                SP  - 22457
                EP  - 22494
                PY  - 
                AB  - Despite a strong genetic background in cognitive function only a limited number of single nucleotide polymorphisms (SNPs) have been found in genome-wide association studies (GWASs). We hypothesize that this is partially due to mis-specified modeling concerning phenotype distribution as well as the relationship between SNP dosage and the level of the phenotype. To overcome these issues, we introduced an assumption-free method based on generalized correlation coefficient (GCC) in a GWAS of cognitive function in Danish and Chinese twins to compare its performance with traditional linear models. The GCC-based GWAS identified two significant SNPs in Danish samples (rs71419535, p = 1.47e-08; rs905838, p = 1.69e-08) and two significant SNPs in Chinese samples (rs2292999, p = 9.27e-10; rs17019635, p = 2.50e-09). In contrast, linear models failed to detect any genome-wide significant SNPs. The number of top significant genes overlapping between the two samples in the GCC-based GWAS was higher than when applying linear models. The GCC model identified significant genetic variants missed by conventional linear models, with more replicated genes and biological pathways related to cognitive function. Moreover, the GCC-based GWAS was robust in handling correlated samples like twin pairs. GCC is a useful statistical method for GWAS that complements traditional linear models for capturing genetic effects beyond the additive assumption.
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Cell differentiation and aging accompanied by depletion of the ACE2 protein

Eva Bártová, Soňa Legartová, Jana Krejčí, Orazio Angelo Arcidiacono,

https://doi.org/10.18632/aging.202221 pp 22495—22508

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Bártová E, Legartová S, Krejčí J, Arcidiacono OA, . Cell differentiation and aging accompanied by depletion of the ACE2 protein. . 12:22495-22508. https://doi.org/10.18632/aging.202221

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                TY  - JOUR
                AU  - Bártová, Eva 
                AU  - Legartová, Soňa 
                AU  - Krejčí, Jana 
                AU  - Arcidiacono, Orazio Angelo 
                TI  - Cell differentiation and aging accompanied by depletion of the ACE2 protein
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202221
                DO  - 10.18632/aging.202221
                SP  - 22495
                EP  - 22508
                PY  - 
                AB  - ACE2 was observed as the cell surface receptor of the SARS-CoV-2 virus. Interestingly, we also found ACE2 positivity inside the cell nucleus. The ACE2 levels changed during cell differentiation and aging and varied in distinct cell types. We observed ACE2 depletion in the aortas of aging female mice, similarly, the aging caused ACE2 decrease in the kidneys. Compared with that in the heart, brain and kidneys, the ACE2 level was the lowest in the mouse lungs. In mice exposed to nicotine, ACE2 was not changed in olfactory bulbs but in the lungs, ACE2 was upregulated in females and downregulated in males. These observations indicate the distinct gender-dependent properties of ACE2.
                Differentiation into enterocytes, and cardiomyocytes, caused ACE2 depletion. The cardiomyogenesis was accompanied by renin upregulation, delayed in HDAC1-depleted cells. In contrast, vitamin D2 decreased the renin level while ACE2 was upregulated. Together, the ACE2 level is high in non-differentiated cells. This protein is more abundant in the tissues of mouse embryos and young mice in comparison with older animals. Mostly, downregulation of ACE2 is accompanied by renin upregulation. Thus, the pathophysiology of COVID-19 disease should be further studied not only by considering the ACE2 level but also the whole renin-angiotensin system.
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Comprehensive characterization of the tumor microenvironment for assessing immunotherapy outcome in patients with head and neck squamous cell carcinoma

Jian Zhang, Xi Zhong, Huali Jiang, Hualong Jiang, Tao Xie, Yunhong Tian, Rong Li, Baiyao Wang, Jiexia Zhang, Yawei Yuan,

https://doi.org/10.18632/aging.103460 pp 22509—22526

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Zhang J, Zhong X, Jiang H, Jiang H, Xie T, Tian Y, Li R, Wang B, Zhang J, Yuan Y, . Comprehensive characterization of the tumor microenvironment for assessing immunotherapy outcome in patients with head and neck squamous cell carcinoma. . 12:22509-22526. https://doi.org/10.18632/aging.103460

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                TY  - JOUR
                AU  - Zhang, Jian 
                AU  - Zhong, Xi 
                AU  - Jiang, Huali 
                AU  - Jiang, Hualong 
                AU  - Xie, Tao 
                AU  - Tian, Yunhong 
                AU  - Li, Rong 
                AU  - Wang, Baiyao 
                AU  - Zhang, Jiexia 
                AU  - Yuan, Yawei 
                TI  - Comprehensive characterization of the tumor microenvironment for assessing immunotherapy outcome in patients with head and neck squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103460
                DO  - 10.18632/aging.103460
                SP  - 22509
                EP  - 22526
                PY  - 
                AB  - The tumor microenvironment (TME) constitutes a complex milieu of cells and cytokines that maintain equilibrium between tumor progression and prognosis. However, comprehensive analysis of the TME and its clinical significance in head and neck squamous cell carcinoma (HNSCC) remains to be unreported. In this study, based on large-scale RNA sequencing data pertaining to single nucleotide variants (SNVs) and copy number variations (CNVs) in HNSCC patients from The Cancer Genome Atlas database, we analysed subpopulations of infiltrating immune cells and evaluated the role of TME infiltration pattern (TME score) in assessing immunotherapy outcome. TME signature genes involved in several inflammation and immunity signalling pathways were observed in the TME score subtype, which were considered immunosuppressive and potentially responsible for significantly worse prognosis. In comparison with SNV- and CNV-mediated tumor mutation burden, TME score can significantly differentiate between high- and low-risk HNSCC and predict immunotherapy outcome. Our data provide clarity on the comprehensive landscape of interactions between clinical characteristics of HNSCC and tumor-infiltrating immune cells. TME score seems to be a useful biomarker that can predict immunotherapy outcome in HNSCC patients.
                ER  -

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Cationic solid lipid nanoparticles loaded by integrin β1 plasmid DNA attenuates IL-1β-induced apoptosis of chondrocyte

Yuejiang Zhao, Hanwen Chen, Lu Wang, Zhiyuan Guo, Shijie Liu, Simin Luo,

https://doi.org/10.18632/aging.103656 pp 22527—22537

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Zhao Y, Chen H, Wang L, Guo Z, Liu S, Luo S, . Cationic solid lipid nanoparticles loaded by integrin β1 plasmid DNA attenuates IL-1β-induced apoptosis of chondrocyte. . 12:22527-22537. https://doi.org/10.18632/aging.103656

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                TY  - JOUR
                AU  - Zhao, Yuejiang 
                AU  - Chen, Hanwen 
                AU  - Wang, Lu 
                AU  - Guo, Zhiyuan 
                AU  - Liu, Shijie 
                AU  - Luo, Simin 
                TI  - Cationic solid lipid nanoparticles loaded by integrin β1 plasmid DNA attenuates IL-1β-induced apoptosis of chondrocyte
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103656
                DO  - 10.18632/aging.103656
                SP  - 22527
                EP  - 22537
                PY  - 
                AB  - Aging-related inflammation is tightly linked with the development of osteoarthritis (OA). As the pro-inflammatory cytokine, IL-1&#x3B2; has been associated with physical dysfunction and frailty. It is still elusive whether and how IL-1&#x3B2; blockade improves the outcome of OA. Here we develop a cationic solid lipid nanoparticles (SLNs) system that effectively mediate non-viral delivery of plasmid DNA (pDNA) into cells. Compared with other DNA transfer technologies including lipofetamin 2000, SLNs-pDNA system is less toxic and exerts identical effectiveness on DNA transfer. Loaded with integrin &#x3B2;1 overexpression pDNA, the SLNs-pDNA mainly localized in cytoplasm and enforced expression of integrin &#x3B2;1 in rat chondrocytes. Moreover, upon exposure to IL-1&#x3B2; stimulation, SLNs-pDNA treatment attenuates the apoptosis rat chondrocytes and augments tissue repair. Our data thus demonstrate that SLNs-pDNA functions as a potential therapeutic nanomedicine in the treatment of osteoarthritis.
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Inflammatory factors and amyloid β-induced microglial polarization promote inflammatory crosstalk with astrocytes

Lushuang Xie, Ning Zhang, Qun Zhang, Chenyu Li, Aaron F. Sandhu, George Williams III, Sirui Lin, PeiRan Lv, Yi Liu, Qiaofeng Wu, Shuguang Yu,

https://doi.org/10.18632/aging.103663 pp 22538—22549

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Xie L, Zhang N, Zhang Q, Li C, Sandhu AF, III GW, Lin S, Lv P, Liu Y, Wu Q, Yu S, . Inflammatory factors and amyloid β-induced microglial polarization promote inflammatory crosstalk with astrocytes. . 12:22538-22549. https://doi.org/10.18632/aging.103663

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                TY  - JOUR
                AU  - Xie, Lushuang 
                AU  - Zhang, Ning 
                AU  - Zhang, Qun 
                AU  - Li, Chenyu 
                AU  - Sandhu, Aaron F. 
                AU  - III, George Williams 
                AU  - Lin, Sirui 
                AU  - Lv, PeiRan 
                AU  - Liu, Yi 
                AU  - Wu, Qiaofeng 
                AU  - Yu, Shuguang 
                TI  - Inflammatory factors and amyloid β-induced microglial polarization promote inflammatory crosstalk with astrocytes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103663
                DO  - 10.18632/aging.103663
                SP  - 22538
                EP  - 22549
                PY  - 
                AB  - The immunological responses are a key pathological factor in Alzheimer&#x2019;s disease (AD). We hypothesized that microglial polarization alters microglia-astrocyte immune interactions in AD. M1 and M2 microglia were isolated from primary rat microglia and were confirmed to secrete pro-inflammatory and anti-inflammatory factors, respectively. Primary rat astrocytes were co-cultured with M1 or M2 microglial medium. M1 microglial medium increased astrocyte production of pro-inflammatory factors (interleukin [IL]-1&#x3B2;, tumor necrosis factor &#x3B1; and IL-6), while M2 microglial medium enhanced astrocyte production of anti-inflammatory factors (IL-4 and IL-10). To analyze the crosstalk between microglia and astrocytes after microglial polarization specifically in AD, we co-cultured astrocytes with medium from microglia treated with amyloid-&#x3B2; (A&#x3B2;) alone or in combination with other inflammatory substances. A&#x3B2; alone and A&#x3B2; combined with lipopolysaccharide/interferon-&#x3B3; induced pro-inflammatory activity in M1 microglia and astrocytes, whereas IL-4/IL-13 inhibited A&#x3B2;-induced pro-inflammatory activity. Nuclear factor &#x3BA;B p65 was upregulated in M1 microglia and pro-inflammatory astrocytes, while Stat6 was upregulated in M2 microglia and anti-inflammatory astrocytes. These results provide direct evidence that microglial polarization governs communication between microglia and astrocytes, and that AD debris alters this crosstalk.
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The therapeutic value of XL388 in human glioma cells

Shan Zhong, Jun Xue, Jiao-Jiao Cao, Bomin Sun, Qing-Fang Sun, Liu-Guan Bian, Liang-Yun Hu, Si-Jian Pan,

https://doi.org/10.18632/aging.103791 pp 22550—22563

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Zhong S, Xue J, Cao J, Sun B, Sun Q, Bian L, Hu L, Pan S, . The therapeutic value of XL388 in human glioma cells. . 12:22550-22563. https://doi.org/10.18632/aging.103791

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                TY  - JOUR
                AU  - Zhong, Shan 
                AU  - Xue, Jun 
                AU  - Cao, Jiao-Jiao 
                AU  - Sun, Bomin 
                AU  - Sun, Qing-Fang 
                AU  - Bian, Liu-Guan 
                AU  - Hu, Liang-Yun 
                AU  - Pan, Si-Jian 
                TI  - The therapeutic value of XL388 in human glioma cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103791
                DO  - 10.18632/aging.103791
                SP  - 22550
                EP  - 22563
                PY  - 
                AB  - XL388 is a highly efficient and orally-available ATP-competitive PI3K-mTOR dual inhibitor. Its activity against glioma cells was studied here. In established and primary human glioma cells, XL388 potently inhibited cell survival and proliferation as well as cell migration, invasion and cell cycle progression. The dual inhibitor induced significant apoptosis activation in glioma cells. In A172 cells and primary human glioma cells, XL388 inhibited Akt-mTORC1/2 activation by blocking phosphorylation of Akt and S6K1. XL388-induced glioma cell death was only partially attenuated by a constitutively-active mutant Akt1. Furthermore, it was cytotoxic against Akt1-knockout A172 glioma cells. XL388 downregulated MAF bZIP transcription factor G (MAFG) and inhibited Nrf2 signaling, causing oxidative injury in glioma cells. Conversely, antioxidants, n-acetylcysteine, pyrrolidine dithiocarbamate and AGI-106, alleviated XL388-induced cytotoxicity and apoptosis in glioma cells. Oral administration of XL388 inhibited subcutaneous A172 xenograft growth in severe combined immunodeficient mice. Akt-S6K1 inhibition and MAFG downregulation were detected in XL388-treated A172 xenograft tissues. Collectively, XL388 efficiently inhibits human glioma cell growth, through Akt-mTOR-dependent and -independent mechanisms.
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Upregulated GDF-15 expression facilitates pancreatic ductal adenocarcinoma progression through orphan receptor GFRAL

Zhiping Zhao, Junfeng Zhang, Liangyu Yin, Jiali Yang, Yao Zheng, Mengjie Zhang, Bing Ni, Huaizhi Wang,

https://doi.org/10.18632/aging.103830 pp 22564—22581

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Zhao Z, Zhang J, Yin L, Yang J, Zheng Y, Zhang M, Ni B, Wang H, . Upregulated GDF-15 expression facilitates pancreatic ductal adenocarcinoma progression through orphan receptor GFRAL. . 12:22564-22581. https://doi.org/10.18632/aging.103830

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                TY  - JOUR
                AU  - Zhao, Zhiping 
                AU  - Zhang, Junfeng 
                AU  - Yin, Liangyu 
                AU  - Yang, Jiali 
                AU  - Zheng, Yao 
                AU  - Zhang, Mengjie 
                AU  - Ni, Bing 
                AU  - Wang, Huaizhi 
                TI  - Upregulated GDF-15 expression facilitates pancreatic ductal adenocarcinoma progression through orphan receptor GFRAL
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103830
                DO  - 10.18632/aging.103830
                SP  - 22564
                EP  - 22581
                PY  - 
                AB  - Growth and differentiation factor 15 (GDF-15) has been studied as an important hallmark of cancer. However, the receptor of GDF-15 in pancreatic cancer cell remains unclear. Here, we investigated its biological effects in pancreatic ductal adenocarcinoma (PDAC). We found that aberrant GDF-15 expression positively correlated with poor survival of PDAC patients. GDF-15 protein enhanced tumor cell proliferation in two pancreatic cancer lines, AsPC-1 and BxPC-3. Knockdown GDF-15 attenuated its biological function in vitro and reduced PDAC cell tumorigenesis upon xenotransplantation into nude mice. Moreover, we identified that glial-derived neurotropic factor family receptor &#x3B1;-like (GFRAL) was upregulated in PDAC tissues and positively correlated with GDF-15 expression. High GFRAL expression was significantly associated with poor survival in PDAC patients. Furthermore, we identified that the biological effects of GDF-15 are mediated by its receptor GFRAL which is present in PDAC cells. After overexpression GFRAL in pancreatic cancer cells, the effect of GDF-15 was significantly enhanced. Overall, our findings demonstrated that the GDF-15 secreted by PDAC cells, binds to GFRAL, itself localized in PDAC cells, to promote cancer cell growth and metastasis through the GDF-15/GFRAL signaling pathway.
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linc00968 inhibits the tumorigenesis and metastasis of lung adenocarcinoma via serving as a ceRNA against miR-9-5p and increasing CPEB3

Huaping Tang, Xiaolei Han, Yan Feng, Yueqin Hao,

https://doi.org/10.18632/aging.103833 pp 22582—22598

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Tang H, Han X, Feng Y, Hao Y, . linc00968 inhibits the tumorigenesis and metastasis of lung adenocarcinoma via serving as a ceRNA against miR-9-5p and increasing CPEB3. . 12:22582-22598. https://doi.org/10.18632/aging.103833

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                TY  - JOUR
                AU  - Tang, Huaping 
                AU  - Han, Xiaolei 
                AU  - Feng, Yan 
                AU  - Hao, Yueqin 
                TI  - linc00968 inhibits the tumorigenesis and metastasis of lung adenocarcinoma via serving as a ceRNA against miR-9-5p and increasing CPEB3
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103833
                DO  - 10.18632/aging.103833
                SP  - 22582
                EP  - 22598
                PY  - 
                AB  - Increasing evidence confirms that long noncoding RNAs (lncRNAs) exert vital functions in multiple biological process among malignant cancers. In the current study, we uncovered that linc00968 was downregulated in lung adenocarcinoma (LUAD). Furthermore, the low level of linc00968 was correlated with worse prognosis in patients with LUAD. Upregulation of linc00968 restrained the growth and metastatic phenotypes of LUAD cell in vitro and in vivo. Using bioinformation methods and luciferase reporter assay, we identified that linc00968 acted as a competing endogenous RNA (ceRNA) via sponging miR-9-5p to modulate the level of Cytoplasmic Polyadenylation Element Binding Protein 3 (CPEB3) in LUAD. In addition, LUAD cell migration, colony formation and epithelial-mesenchymal transition (EMT) process were suppressed by linc00968 while these aggressive traits were reversed by miR-142-5p or CPEB3 silencing. Altogether, our work disclosed that linc00968 played a critical role in LUAD and linc00968/miR-9-5p/CPEB3 regulatory axis might be a potential treatment target in LUAD.
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miR-25-3p promotes endothelial cell angiogenesis in aging mice via TULA-2/SYK/VEGFR-2 downregulation

Chong Lian, Lei Zhao, Jiacong Qiu, Yang Wang, Rencong Chen, Zhen Liu, Jin Cui, Xiaonan Zhu, Xuejun Wen, Shenming Wang, Jinsong Wang,

https://doi.org/10.18632/aging.103834 pp 22599—22613

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Lian C, Zhao L, Qiu J, Wang Y, Chen R, Liu Z, Cui J, Zhu X, Wen X, Wang S, Wang J, . miR-25-3p promotes endothelial cell angiogenesis in aging mice via TULA-2/SYK/VEGFR-2 downregulation. . 12:22599-22613. https://doi.org/10.18632/aging.103834

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                TY  - JOUR
                AU  - Lian, Chong 
                AU  - Zhao, Lei 
                AU  - Qiu, Jiacong 
                AU  - Wang, Yang 
                AU  - Chen, Rencong 
                AU  - Liu, Zhen 
                AU  - Cui, Jin 
                AU  - Zhu, Xiaonan 
                AU  - Wen, Xuejun 
                AU  - Wang, Shenming 
                AU  - Wang, Jinsong 
                TI  - miR-25-3p promotes endothelial cell angiogenesis in aging mice via TULA-2/SYK/VEGFR-2 downregulation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103834
                DO  - 10.18632/aging.103834
                SP  - 22599
                EP  - 22613
                PY  - 
                AB  - In aging, the regulation of angiogenesis is a dynamic and complex process. We aimed to identify and characterize microRNAs that regulate angiogenesis during aging. We showed that, in response to vascular endothelial senescence, microRNA-25-3p (miR-25-3p) plays the role of an angiogenic microRNA by targeting TULA-2 (T-cell ubiquitin ligand-2)/SYK (spleen tyrosine kinase)/VEGFR-2 (vascular endothelial growth factor receptor 2) signaling in vitro and in vivo. Mechanistic studies demonstrated that miR-25-3p inhibits a TULA-2/SYK/VEGFR-2 signaling pathway in endothelial cells. In old endothelial cells (OECs), upregulation of miR-25-3p inhibited the expression of TULA-2, which caused downregulation of the interaction between TULA-2 and SYK and increased phosphorylation of SYK Y323. The increased SYK Y323 phosphorylation level upregulated the phosphorylation of VEGFR-2 Y1175, which plays a vital role in angiogenesis, while miR-25-3p downregulation in YECs showed opposite effects. Finally, a salvage study showed that miR-25-3p upregulation promoted capillary regeneration and hindlimb blood flow recovery in aging mice with hindlimb ischemia. These findings suggest that miR-25-3p acts as an agonist of TULA-2/SYK/VEGFR-2 and mediates the endothelial cell angiogenesis response, which shows that the miR-25-3p/TULA-2 pathway may be potential therapeutic targets for angiogenesis during aging.
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The relationship between activities of daily living and suicidal ideation among Chinese rural older adults: a multiple mediation model through sleep quality and psychological distress

Dan Zhao, Jie Li, Wenting Hao, Yemin Yuan, Caiting Yu, Zhengyue Jing, Yi Wang, Peipei Fu, Chengchao Zhou,

https://doi.org/10.18632/aging.103857 pp 22614—22625

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Zhao D, Li J, Hao W, Yuan Y, Yu C, Jing Z, Wang Y, Fu P, Zhou C, . The relationship between activities of daily living and suicidal ideation among Chinese rural older adults: a multiple mediation model through sleep quality and psychological distress. . 12:22614-22625. https://doi.org/10.18632/aging.103857

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                TY  - JOUR
                AU  - Zhao, Dan 
                AU  - Li, Jie 
                AU  - Hao, Wenting 
                AU  - Yuan, Yemin 
                AU  - Yu, Caiting 
                AU  - Jing, Zhengyue 
                AU  - Wang, Yi 
                AU  - Fu, Peipei 
                AU  - Zhou, Chengchao 
                TI  - The relationship between activities of daily living and suicidal ideation among Chinese rural older adults: a multiple mediation model through sleep quality and psychological distress
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103857
                DO  - 10.18632/aging.103857
                SP  - 22614
                EP  - 22625
                PY  - 
                AB  - Few studies clarified the mechanisms underlying the relationship between activities of daily living and suicidal ideation among older adults. This study aimed to explore the multiple mediating roles of sleep quality and psychological distress between this relationship. A total of 3,243 rural older adults were included. Multiple mediation analysis was performed using Mplus 8.3. Activities of daily living was found to directly affect suicidal ideation (&#x3B2;=0.092, 95% CI=0.043&#x2212;0.140) and through three significantly mediation pathways: (1) the path through sleep quality (&#x3B2;=0.019, 95% CI=0.007&#x2212;0.031), which accounted for 9.79 % of the total effect; (2) the path through psychological distress (&#x3B2;=0.049, 95% CI=0.036&#x2212;0.063), which accounted for 25.26 % of the total effect; (3) the path through sleep quality and psychological distress (&#x3B2;=0.034, 95% CI=0.026&#x2212;0.042), which accounted for 17.53 % of the total effect. The total mediating effect was 52.58%. Attention should be paid to sleep quality and mental health among the Chinese rural older adults with activities of daily living limitation. For early detection and prevention of suicidal ideation, it is necessary to take sleep-based and positive psychological interventions for older adults with activities of daily living limitation.
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Colon cancer-specific diagnostic and prognostic biomarkers based on genome-wide abnormal DNA methylation

Yilin Wang, Ming Zhang, Xiaoyun Hu, Wenyan Qin, Huizhe Wu, Minjie Wei,

https://doi.org/10.18632/aging.103874 pp 22626—22655

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Wang Y, Zhang M, Hu X, Qin W, Wu H, Wei M, . Colon cancer-specific diagnostic and prognostic biomarkers based on genome-wide abnormal DNA methylation. . 12:22626-22655. https://doi.org/10.18632/aging.103874

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                TY  - JOUR
                AU  - Wang, Yilin 
                AU  - Zhang, Ming 
                AU  - Hu, Xiaoyun 
                AU  - Qin, Wenyan 
                AU  - Wu, Huizhe 
                AU  - Wei, Minjie 
                TI  - Colon cancer-specific diagnostic and prognostic biomarkers based on genome-wide abnormal DNA methylation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103874
                DO  - 10.18632/aging.103874
                SP  - 22626
                EP  - 22655
                PY  - 
                AB  - Abnormal DNA methylation is a major early contributor to colon cancer (COAD) development. We conducted a cohort-based systematic investigation of genome-wide DNA methylation using 299 COAD and 38 normal tissue samples from TCGA. Through conditional screening and machine learning with a training cohort, we identified one hypomethylated and nine hypermethylated differentially methylated CpG sites as potential diagnostic biomarkers, and used them to construct a COAD-specific diagnostic model. Unlike previous models, our model precisely distinguished COAD from nine other cancer types (e.g., breast cancer and liver cancer; error rate &#x2264; 0.05) and from normal tissues in the training cohort (AUC = 1). The diagnostic model was verified using a validation cohort from The Cancer Genome Atlas (AUC = 1) and five independent cohorts from the Gene Expression Omnibus (AUC &#x2265; 0.951). Using Cox regression analyses, we established a prognostic model based on six CpG sites in the training cohort, and verified the model in the validation cohort. The prognostic model sensitively predicted patients&#x2019; survival (p &#x2264; 0.00011, AUC &#x2265; 0.792) independently of important clinicopathological characteristics of COAD (e.g., gender and age). Thus, our DNA methylation analysis provided precise biomarkers and models for the early diagnosis and prognostic evaluation of COAD.
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Long non-coding RNA ZFAS1 promotes colorectal cancer tumorigenesis and development through DDX21-POLR1B regulatory axis

Xiufang Wang, Zhikun Wu, Wenyan Qin, Tong Sun, Senxu Lu, Yalun Li, Yuanhe Wang, Xiaoyun Hu, Dongping Xu, Yutong Wu, Qiuchen Chen, Weifan Yao, Mingyan Liu, Minjie Wei, Huizhe Wu,

https://doi.org/10.18632/aging.103875 pp 22656—22687

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Wang X, Wu Z, Qin W, Sun T, Lu S, Li Y, Wang Y, Hu X, Xu D, Wu Y, Chen Q, Yao W, Liu M, et al, . Long non-coding RNA ZFAS1 promotes colorectal cancer tumorigenesis and development through DDX21-POLR1B regulatory axis. . 12:22656-22687. https://doi.org/10.18632/aging.103875

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                TY  - JOUR
                AU  - Wang, Xiufang 
                AU  - Wu, Zhikun 
                AU  - Qin, Wenyan 
                AU  - Sun, Tong 
                AU  - Lu, Senxu 
                AU  - Li, Yalun 
                AU  - Wang, Yuanhe 
                AU  - Hu, Xiaoyun 
                AU  - Xu, Dongping 
                AU  - Wu, Yutong 
                AU  - Chen, Qiuchen 
                AU  - Yao, Weifan 
                AU  - Liu, Mingyan 
                AU  - Wei, Minjie 
                AU  - Wu, Huizhe 
                TI  - Long non-coding RNA ZFAS1 promotes colorectal cancer tumorigenesis and development through DDX21-POLR1B regulatory axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103875
                DO  - 10.18632/aging.103875
                SP  - 22656
                EP  - 22687
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wang, Xiufang 
                AU  - Wu, Zhikun 
                AU  - Qin, Wenyan 
                AU  - Sun, Tong 
                AU  - Lu, Senxu 
                AU  - Li, Yalun 
                AU  - Wang, Yuanhe 
                AU  - Hu, Xiaoyun 
                AU  - Xu, Dongping 
                AU  - Wu, Yutong 
                AU  - Chen, Qiuchen 
                AU  - Yao, Weifan 
                AU  - Liu, Mingyan 
                AU  - Wei, Minjie 
                AU  - Wu, Huizhe 
                TI  - Long non-coding RNA ZFAS1 promotes colorectal cancer tumorigenesis and development through DDX21-POLR1B regulatory axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103875
                DO  - 10.18632/aging.103875
                SP  - 22656
                EP  - 22687
                PY  - 
                AB  - Increasing evidence supports long non-coding RNA-ZFAS1 as master protein regulators involved in a variety of human cancers. However, the molecular mechanism is not fully understood in colorectal cancer (CRC) and remains to be elucidated. Here, we uncovered a previously unreported mechanism linking RNA helicase DDX21 regulated by lncRNA ZFAS1 in control of POLR1B expression in CRC initiation and progression. Specifically, ZFAS1 exerted its oncogenic functions and was significantly up-regulated accompanied by elevated DDX21, POLR1B expression in CRC cells and tissues, which further closely associated with poor clinical outcomes. Notably, ZFAS1 knockdown dramatically suppressed CRC cell proliferation, invasion, migration, and increased cell apoptosis, which were contrary to the effect caused by ZFAS1 up-regulation. We further revealed that the inhibitory effect caused by ZFAS1 knockdown could be reversed by DDX21 overexpression in vitro and in vivo. Mechanistically, our research found that ZFAS1 could directly recruit DDX21 protein by harboring the specific motif (AAGA or CAGA). Finally, POLR1B was identified as the downstream target of DDX21 regulated by ZFAS1, which was also up-regulated in CRC cells and tissues and closely related to poor prognosis. The unrecognized ZFAS1/DDX21/POLR1B signaling regulation axis may provide new biomarkers and targets for CRC treatment and prognostic evaluation.
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Glycemic traits and Alzheimer’s disease: a Mendelian randomization study

Yuesong Pan, Weiqi Chen, Hongyi Yan, Mengxing Wang, Xianglong Xiang,

https://doi.org/10.18632/aging.103887 pp 22688—22699

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Pan Y, Chen W, Yan H, Wang M, Xiang X, . Glycemic traits and Alzheimer’s disease: a Mendelian randomization study. . 12:22688-22699. https://doi.org/10.18632/aging.103887

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                TY  - JOUR
                AU  - Pan, Yuesong 
                AU  - Chen, Weiqi 
                AU  - Yan, Hongyi 
                AU  - Wang, Mengxing 
                AU  - Xiang, Xianglong 
                TI  - Glycemic traits and Alzheimer’s disease: a Mendelian randomization study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103887
                DO  - 10.18632/aging.103887
                SP  - 22688
                EP  - 22699
                PY  - 
                AB  - Previous observational studies have reported an association between impaired glucose metabolism and Alzheimer&#x2019;s disease. This study aimed to examine the causal association of glycemic traits with Alzheimer&#x2019;s disease. We used a two-sample Mendelian randomization approach to evaluate the causal effect of six glycemic traits (type 2 diabetes, fasting glucose, fasting insulin, hemoglobin A1c, homeostasis model assessment- insulin resistance and HOMA-&#x3B2;-cell function) on Alzheimer&#x2019;s disease. Summary data on the association of single nucleotide polymorphisms with these glycemic traits were obtained from genome-wide association studies of the DIAbetes Genetics Replication And Meta-analysis and Meta-Analyses of Glucose and Insulin-related traits Consortium. Summary data on the association of single nucleotide polymorphisms with Alzheimer&#x2019;s disease were obtained from the International Genomics of Alzheimer&apos;s Project. The Mendelian randomization analysis showed that 1-standard deviation higher fasting glucose and lower HOMA-&#x3B2;-cell function (indicating pancreatic &#x3B2;-cell dysfunction) were causally associated with a substantial increase in risk of Alzheimer&#x2019;s disease (odds ratio=1.33, 95% confidence interval: 1.04-1.68, p=0.02; odds ratio=1.92, 95% confidence interval: 1.15-3.21, p=0.01). However, no significant association was observed for other glycemic traits. This Mendelian randomization analysis provides evidence of causal associations between glycemic traits, especially high fasting glucose and pancreatic &#x3B2;-cell dysfunction, and high risk of Alzheimer&apos;s disease.
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Drug-selected population in melanoma A2058 cells as melanoma stem-like cells retained angiogenic features – the potential roles of heparan-sulfate binding ANGPTL4 protein

Chia-Yu Shih, Yu-Che Cheng, ChiaoHui Hsieh, TingTing Tseng, ShihSheng Jiang, Shao-Chen Lee,

https://doi.org/10.18632/aging.103890 pp 22700—22718

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Shih C, Cheng Y, Hsieh C, Tseng T, Jiang S, Lee S, . Drug-selected population in melanoma A2058 cells as melanoma stem-like cells retained angiogenic features – the potential roles of heparan-sulfate binding ANGPTL4 protein. . 12:22700-22718. https://doi.org/10.18632/aging.103890

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                TY  - JOUR
                AU  - Shih, Chia-Yu 
                AU  - Cheng, Yu-Che 
                AU  - Hsieh, ChiaoHui 
                AU  - Tseng, TingTing 
                AU  - Jiang, ShihSheng 
                AU  - Lee, Shao-Chen 
                TI  - Drug-selected population in melanoma A2058 cells as melanoma stem-like cells retained angiogenic features – the potential roles of heparan-sulfate binding ANGPTL4 protein
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103890
                DO  - 10.18632/aging.103890
                SP  - 22700
                EP  - 22718
                PY  - 
                AB  - Malignant cancer may contain highly heterogeneous populations of cells, including stem-like cells which were resistant to chemotherapy agents, radiation, mechanical stress, and immune surveillance. The characterization of these specific subpopulations might be critical to develop novel strategy to remove malignant tumors.
                We selected and enriched small population of human melanoma A2058 cells by repetitive selection cycles (selection, restoration, and amplification). These subpopulation of melanoma cells persisted the characteristics of slower cell proliferation, enhanced drug-resistance, elevated percentage of side population as analyzed by Hoechst33342 exclusion, in vitro sphere formation, and in vivo xenograft tumor formation by small amount of tumor cells. The selected populations would be melanoma stem-like cells with high expression of stem cell markers and altered kinase activation. Microarray and bioinformatics analysis highlighted the high expression of angiopoietin-like 4 protein in drug-selected melanoma stem-like cells. Further validation by specific shRNA demonstrated the role of angiopoietin-like 4 protein in drug-selected subpopulation associated with enhanced drug-resistance, sphere formation, reduced kinase activation, in vitro tube-forming ability correlated with heparan-sulfate proteoglycans.
                Our finding would be applicable to explore the mechanism of melanoma stemness and use angiopoietin-like 4 as potential biomarkers to identify melanoma stem-like cells.
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Gonadal white adipose tissue-derived exosomal MiR-222 promotes obesity-associated insulin resistance

Dameng Li, Huichen Song, Linghu Shuo, Lei Wang, Ping Xie, Weili Li, Jiachen Liu, Yafei Tong, Chen-Yu Zhang, Xiaohong Jiang, Jing Li, Yujing Zhang,

https://doi.org/10.18632/aging.103891 pp 22719—22743

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Li D, Song H, Shuo L, Wang L, Xie P, Li W, Liu J, Tong Y, Zhang C, Jiang X, Li J, Zhang Y, . Gonadal white adipose tissue-derived exosomal MiR-222 promotes obesity-associated insulin resistance. . 12:22719-22743. https://doi.org/10.18632/aging.103891

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                TY  - JOUR
                AU  - Li, Dameng 
                AU  - Song, Huichen 
                AU  - Shuo, Linghu 
                AU  - Wang, Lei 
                AU  - Xie, Ping 
                AU  - Li, Weili 
                AU  - Liu, Jiachen 
                AU  - Tong, Yafei 
                AU  - Zhang, Chen-Yu 
                AU  - Jiang, Xiaohong 
                AU  - Li, Jing 
                AU  - Zhang, Yujing 
                TI  - Gonadal white adipose tissue-derived exosomal MiR-222 promotes obesity-associated insulin resistance
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103891
                DO  - 10.18632/aging.103891
                SP  - 22719
                EP  - 22743
                PY  - 
                AB  - In this study, we investigated the role of serum exosomal miR-222 in obesity-related insulin resistance. Bioinformatics analyses showed that miR-222 levels were significantly upregulated in the white adipose tissue of obese patients with insulin resistance (GSE25402 dataset) and in serum samples from type 2 diabetes mellitus (T2DM) patients (GSE90028 dataset). Moreover, analysis of miRNA expression in adipose tissue-specific Dicer knockout mice (GitHub dataset) and diabetic model mice (GSE81976 and GSE85101 datasets), gonadal white adipose tissue (gWAT) was the main source of serum exosomal miR-222. MiR-222 levels were significantly elevated in the serum, serum exosomes and gWAT of mice fed a high-fat diet (HFD), and there was a corresponding downregulation of IRS1 and phospho-AKT levels in their liver and skeletal muscle tissues, which correlated with impaired insulin sensitivity and glucose intolerance. These effects were abrogated by surgically removing the gWAT from the HFD-fed mice. Thus, gWAT-derived serum exosomal miR-222 appears to promote insulin resistance in the liver and skeletal muscle of HFD-fed obese mice by suppressing IRS1 expression.
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Geniposide ameliorated sepsis-induced acute kidney injury by activating PPARγ

Jinhong Liu, Ning Zhao, Guiling Shi, Hai Wang,

https://doi.org/10.18632/aging.103902 pp 22744—22758

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Liu J, Zhao N, Shi G, Wang H, . Geniposide ameliorated sepsis-induced acute kidney injury by activating PPARγ. . 12:22744-22758. https://doi.org/10.18632/aging.103902

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                TY  - JOUR
                AU  - Liu, Jinhong 
                AU  - Zhao, Ning 
                AU  - Shi, Guiling 
                AU  - Wang, Hai 
                TI  - Geniposide ameliorated sepsis-induced acute kidney injury by activating PPARγ
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103902
                DO  - 10.18632/aging.103902
                SP  - 22744
                EP  - 22758
                PY  - 
                AB  - Acute kidney injury is one of the most common complications that occurs in septic shock. An effective therapeutic intervention is urgently needed. Geniposide has been reported to possess pleiotropic activities against different diseases. However, the effect of geniposide on sepsis-induced kidney injury is unexplored. Our study aims to illustrate the mitigative effects of geniposide on sepsis-induced kidney injury and its relevant mechanisms. Sepsis was induced in mice undergoing cecal ligation and puncture (CLP) surgery. Mice were intraperitoneally injected with geniposide (10, 20 and 40 mg/kg) for treatment. The results showed that geniposide ameliorated kidney injury and dysfunction in CLP-induced septic mice, accompanied by reduction of inflammatory response and oxidative stress. We also found that geniposide significantly reduced vascular permeability and cellular apoptosis of the kidney, with increase of Bcl-2 and decrease of Bax and cleaved caspase-3. Moreover, PPAR&#x3B3; was found to be upregulated with the increasing concentration of geniposide. The protection of geniposide against inflammation and apoptosis was recovered by inhibition of PPAR&#x3B3;. Collectively, these results indicate that geniposide could significantly ameliorate acute kidney injury in CLP-induced septic mice and LPS-stimulated HK-2 cells by activating PPAR&#x3B3;. Geniposide might be a potential drug candidate for sepsis-induced kidney injury.
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NEAT1/miR-200b-3p/SMAD2 axis promotes progression of melanoma

Wen-Jie Zhou, Hao-Yu Wang, Jie Zhang, Hai-Ying Dai, Zhi-Xian Yao, Zhong Zheng, Sun Meng-Yan, Ke Wu,

https://doi.org/10.18632/aging.103909 pp 22759—22775

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Zhou W, Wang H, Zhang J, Dai H, Yao Z, Zheng Z, Meng-Yan S, Wu K, . NEAT1/miR-200b-3p/SMAD2 axis promotes progression of melanoma. . 12:22759-22775. https://doi.org/10.18632/aging.103909

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                TY  - JOUR
                AU  - Zhou, Wen-Jie 
                AU  - Wang, Hao-Yu 
                AU  - Zhang, Jie 
                AU  - Dai, Hai-Ying 
                AU  - Yao, Zhi-Xian 
                AU  - Zheng, Zhong 
                AU  - Meng-Yan, Sun 
                AU  - Wu, Ke 
                TI  - NEAT1/miR-200b-3p/SMAD2 axis promotes progression of melanoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103909
                DO  - 10.18632/aging.103909
                SP  - 22759
                EP  - 22775
                PY  - 
                AB  - Melanoma is a skin malignancy with a high mutation frequency of genetic alterations. MicroRNA (miR)-200b-3p is involved in various cancers, while in melanoma its bio-function remains unknown. In this study, we found that miR-200b-3p was down-regulated in melanoma tissues and cell lines compared to benign nevus cells. Overexpression of miR-200b-3p significantly inhibited the proliferation and invasion of melanoma cells. According to bioinformatics analysis and sequencing data, we supposed that SMAD family member 2 (SMAD2) was the target gene and nuclear enriched abundant transcript 1 (NEAT1) was the upstream long non-coding RNA (lncRNA) of miR-200b-3p. These predictions were verified by western blotting and quantitative real-time reverse transcription PCR (RT-qPCR). Luciferase reporter assays revealed that NEAT1 up-regulated SMAD2 by directly sponging miR-200b-3p. In vitro and in vivo, we demonstrated that both NEAT1 and SMAD2 could promote the proliferation and invasion of melanoma cells, and these effects were reversed by up-regulating miR-200b-3p. In addition, NEAT1/miR-200b-3p/SMAD2 axis promoted melanoma progression by activating EMT signaling pathway and immune responses. Taken together, the NEAT1/miR-200b-3p/SMAD2 signaling pathway promotes melanoma via activation of EMT, cell invasion and is related with immune responses, which provides new insights into the molecular mechanisms and therapeutic targets for melanoma.
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Immune-related biomarker risk score predicts prognosis in prostate cancer

Zezhen Liu, Jiehui Zhong, Chao Cai, Jianming Lu, Wenqi Wu, Guohua Zeng,

https://doi.org/10.18632/aging.103921 pp 22776—22793

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Liu Z, Zhong J, Cai C, Lu J, Wu W, Zeng G, . Immune-related biomarker risk score predicts prognosis in prostate cancer. . 12:22776-22793. https://doi.org/10.18632/aging.103921

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                TY  - JOUR
                AU  - Liu, Zezhen 
                AU  - Zhong, Jiehui 
                AU  - Cai, Chao 
                AU  - Lu, Jianming 
                AU  - Wu, Wenqi 
                AU  - Zeng, Guohua 
                TI  - Immune-related biomarker risk score predicts prognosis in prostate cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103921
                DO  - 10.18632/aging.103921
                SP  - 22776
                EP  - 22793
                PY  - 
                AB  - In this study, we constructed a model using a Cox proportional hazards model based on the expression of eight immune-related genes that were associated with prognosis in prostate cancer: EDNRB, ANGPTL2, TNFSF15, TNFRSF10D, EDN2, BMP2, NLRP14, and PLK1. We then identified associations between risk scores calculated with the model, tumor microenvironment characteristics, and immune cell infiltration. Prostate cancer patients in the high score group had poorer prognoses, and validation with the external GSE54460 dataset confirmed that the scoring model predicted biochemical recurrence with AUC values of 0.749 at 1 year, 0.804 at 3 years, and 0.774 at 5 years. Proportions of infiltrated M2 macrophages and regulatory T cells were increased in the high risk group, while CD8+ T cells were increased in the low risk group. Network analysis revealed that PLK1 may be a key regulator of the immune-suppressive microenvironment in prostate cancer. Double immunofluorescence labeling of a prostate cancer tissue microarray indicated that PLK1 expression correlated positively with numbers of infiltrating macrophages. These results indicate that an immune- related, gene-based risk score effectively reflects immune microenvironment characteristics and predicts prognosis in prostate cancer.
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Integrative analysis of transcriptomes highlights potential functions of transfer-RNA-derived small RNAs in experimental intracerebral hemorrhage

Peng-Fei Li, Shi-Chao Guo, Tao Liu, Hanjin Cui, Dandan Feng, Ali Yang, Zhe Cheng, Jiekun Luo, Tao Tang, Yang Wang,

https://doi.org/10.18632/aging.103938 pp 22794—22813

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Li P, Guo S, Liu T, Cui H, Feng D, Yang A, Cheng Z, Luo J, Tang T, Wang Y, . Integrative analysis of transcriptomes highlights potential functions of transfer-RNA-derived small RNAs in experimental intracerebral hemorrhage. . 12:22794-22813. https://doi.org/10.18632/aging.103938

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                TY  - JOUR
                AU  - Li, Peng-Fei 
                AU  - Guo, Shi-Chao 
                AU  - Liu, Tao 
                AU  - Cui, Hanjin 
                AU  - Feng, Dandan 
                AU  - Yang, Ali 
                AU  - Cheng, Zhe 
                AU  - Luo, Jiekun 
                AU  - Tang, Tao 
                AU  - Wang, Yang 
                TI  - Integrative analysis of transcriptomes highlights potential functions of transfer-RNA-derived small RNAs in experimental intracerebral hemorrhage
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103938
                DO  - 10.18632/aging.103938
                SP  - 22794
                EP  - 22813
                PY  - 
                AB  - Transfer-RNA-derived small RNAs (tsRNAs) are a novel class of short non-coding RNAs, that possess regulatory functions. However, their biological roles in hemorrhagic stroke are not understood. In this study, by RNA sequencing, we investigated the tsRNA expression profiles of intracerebral hemorrhagic rat brains in the chronic phase. A total of 331 tsRNAs were identified (308 in sham and 309 in intracerebral hemorrhage). Among them, the validation revealed that 7 tsRNAs (1 up-regulated and 6 down-regulated) were significantly changed. Subsequently, we predicted the target mRNAs of the 7 tsRNAs. Through integrative analysis, the predicted targets were validated by mRNA microarray data. Moreover, we confirmed the functions of tsRNAs targeting mRNAs in vitro. Furthermore, using bioinformatics tools and databases, we developed a tsRNA-mRNA-pathway interaction network to visualize their potential functions. Bioinformatics analyses and confirmatory experiments indicated that the altered genes were mainly enriched in several signaling pathways. These pathways were interrelated with intracerebral hemorrhage, such as response to oxidative stress, endocytosis, and regulation of G protein-coupled receptor signaling pathway. In summary, this study systematically revealed the profiles of tsRNAs after an experimental intracerebral hemorrhage. These results may provide novel therapeutic targets following a hemorrhagic stroke in the chronic phase.
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Analysis of DNA methylation-driven genes for predicting the prognosis of patients with colorectal cancer

Boshi Fu, Cheng Du, Zhikun Wu, Mingwei Li, Yi Zhao, Xinli Liu, Huizhe Wu, Minjie Wei,

https://doi.org/10.18632/aging.103949 pp 22814—22839

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Fu B, Du C, Wu Z, Li M, Zhao Y, Liu X, Wu H, Wei M, . Analysis of DNA methylation-driven genes for predicting the prognosis of patients with colorectal cancer. . 12:22814-22839. https://doi.org/10.18632/aging.103949

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                TY  - JOUR
                AU  - Fu, Boshi 
                AU  - Du, Cheng 
                AU  - Wu, Zhikun 
                AU  - Li, Mingwei 
                AU  - Zhao, Yi 
                AU  - Liu, Xinli 
                AU  - Wu, Huizhe 
                AU  - Wei, Minjie 
                TI  - Analysis of DNA methylation-driven genes for predicting the prognosis of patients with colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103949
                DO  - 10.18632/aging.103949
                SP  - 22814
                EP  - 22839
                PY  - 
                AB  - Aberrant promoter methylation and ensuing abnormal gene expression are important epigenetic mechanisms that contribute to colorectal oncogenesis. Yet, the prognostic significance of such methylation-driven genes in colorectal cancer (CRC) remains obscure. Herein, a total of 181 genes were identified as the methylation-driven molecular features of CRC by integrated analysis of the expression profiles and the matched DNA methylation data from The Cancer Genome Atlas (TCGA) database. Among them, a five-gene signature (POU4F1, NOVA1, MAGEA1, SLCO4C1, and IZUMO2) was developed as a risk assessment model for predicting the clinical outcomes in CRC. The Kaplan&#x2013;Meier analysis and Harrell&#x2019;s C index demonstrated that the risk assessment model significantly distinguished the patients in high or low-risk groups (p-value &lt; 0.0001 log-rank test, HR: 2.034, 95% CI: 1.419-2.916, C index: 0.655). The sensitivity and specificity were validated by the receiver operating characteristic (ROC) analysis. Furthermore, different pharmaceutical treatment responses were observed between the high-risk and low-risk groups. Indeed, the methylation-driven gene signature could act as an independent prognostic evaluation biomarker for assessing the OS of CRC patients and guiding the pharmaceutical treatment. Compared with known biomarkers, the methylation-driven gene signature could reveal cross-omics molecular features for improving clinical stratification and prognosis.
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Establishing and validating a pathway prognostic signature in pancreatic cancer based on miRNA and mRNA sets using GSVA

Junfeng Zhang, Jianyou Gu, Shixiang Guo, Wenjie Huang, Yao Zheng, Xianxing Wang, Tao Zhang, Weibo Zhao, Bing Ni, Yingfang Fan, Huaizhi Wang,

https://doi.org/10.18632/aging.103965 pp 22840—22858

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Zhang J, Gu J, Guo S, Huang W, Zheng Y, Wang X, Zhang T, Zhao W, Ni B, Fan Y, Wang H, . Establishing and validating a pathway prognostic signature in pancreatic cancer based on miRNA and mRNA sets using GSVA. . 12:22840-22858. https://doi.org/10.18632/aging.103965

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                TY  - JOUR
                AU  - Zhang, Junfeng 
                AU  - Gu, Jianyou 
                AU  - Guo, Shixiang 
                AU  - Huang, Wenjie 
                AU  - Zheng, Yao 
                AU  - Wang, Xianxing 
                AU  - Zhang, Tao 
                AU  - Zhao, Weibo 
                AU  - Ni, Bing 
                AU  - Fan, Yingfang 
                AU  - Wang, Huaizhi 
                TI  - Establishing and validating a pathway prognostic signature in pancreatic cancer based on miRNA and mRNA sets using GSVA
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103965
                DO  - 10.18632/aging.103965
                SP  - 22840
                EP  - 22858
                PY  - 
                AB  - Pancreatic cancer (PC) is a severe disease with the highest mortality rate among various cancers. It is urgent to find an effective and accurate way to predict the survival of PC patients. Gene set variation analysis (GSVA) was used to establish and validate a miRNA set-based pathway prognostic signature for PC (miPPSPC) and a mRNA set-based pathway prognostic signature for PC (mPPSPC) in independent datasets. An optimized miPPSPC was constructed by combining clinical parameters. The miPPSPC, optimized miPPSPC and mPPSPC were established and validated to predict the survival of PC patients and showed excellent predictive ability. Four metabolic pathways and one oxidative stress pathway were identified in the miPPSPC, whereas linoleic acid metabolism and the pentose phosphate pathway were identified in the mPPSPC. Key factors of the pentose phosphate pathway and linoleic acid metabolism, G6PD and CYP2C8/9/18/19, respectively, are related to the survival of PC patients according to our tissue microarray. Thus, the miPPSPC, optimized miPPSPC and mPPSPC can predict the survival of PC patients efficiently and precisely. The metabolic and oxidative stress pathways may participate in PC progression.
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Identification of novel FUS and TARDBP gene mutations in Chinese amyotrophic lateral sclerosis patients with HRM analysis

Feng Wang, Shengyu Fu, Jiafan Lei, Hongchen Wu, Shugui Shi, Kangning Chen, Jun Hu, Xueqing Xu,

https://doi.org/10.18632/aging.103967 pp 22859—22868

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Wang F, Fu S, Lei J, Wu H, Shi S, Chen K, Hu J, Xu X, . Identification of novel FUS and TARDBP gene mutations in Chinese amyotrophic lateral sclerosis patients with HRM analysis. . 12:22859-22868. https://doi.org/10.18632/aging.103967

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Provider: 
 TY - JOUR
 AU - Wang, Feng 
 AU - Fu, Shengyu 
 AU - Lei, Jiafan 
 AU - Wu, Hongchen 
 AU - Shi, Shugui 
 AU - Chen, Kangning 
 AU - Hu, Jun 
 AU - Xu, Xueqing 
 TI - Identification of novel FUS and TARDBP gene mutations in Chinese amyotrophic lateral sclerosis patients with HRM analysis
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103967
 DO - 10.18632/aging.103967
 SP - 22859
 EP - 22868
 PY - 
 AB - Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons. More than 30 genes have been linked to ALS to date, including FUS and TARDBP, which exhibit similar roles in RNA metabolism. This study explored the use of high-resolution melting (HRM) analysis to screen for FUS and TARDBP mutation hotspot regions in 146 Chinese ALS patients, which achieved 100% detection. Two FUS mutations were observed in two different familial ALS probands, a missense mutation (p.R521H) and a novel splicing mutation (c.1541+1G&gt;A). Five TARDBP mutations were identified in six ALS patients, including a novel 3&#x2019;UTR mutation (c.*731A&gt;G) and four missense mutations (p.G294V, p.M337V, p.G348V, and p.I383V). We found that FUS mutations were present in 1.4% of Chinese ALS patients, whereas TARDBP mutations were responsible for 4.1% of Chinese ALS cases. Here, we describe the accuracy of using highly sensitive HRM analysis to identify two novel FUS and TARDBP mutations in Chinese sporadic and familial ALS cases. Our study contributes to the further understanding of the genetic and phenotypic diversity of ALS.
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Global burden and trend of acute lymphoblastic leukemia from 1990 to 2017

Ming Yi, Linghui Zhou, Anping Li, Suxia Luo, Kongming Wu,

https://doi.org/10.18632/aging.103982 pp 22869—22891

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Yi M, Zhou L, Li A, Luo S, Wu K, . Global burden and trend of acute lymphoblastic leukemia from 1990 to 2017. . 12:22869-22891. https://doi.org/10.18632/aging.103982

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                TY  - JOUR
                AU  - Yi, Ming 
                AU  - Zhou, Linghui 
                AU  - Li, Anping 
                AU  - Luo, Suxia 
                AU  - Wu, Kongming 
                TI  - Global burden and trend of acute lymphoblastic leukemia from 1990 to 2017
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103982
                DO  - 10.18632/aging.103982
                SP  - 22869
                EP  - 22891
                PY  - 
                AB  - Acute lymphoblastic leukemia (ALL) is a common malignant hematologic disease that is characterized by large numbers of dedifferentiated lymphoid cells. Statistical data of ALL&apos;s incidence and mortality are fundamental for policymakers to allocate resources optimally. In this study, we reported the incidence, death, and disability-adjusted life year (DALY) of ALL in the globe from 1990 to 2017. Our analysis showed that the incidence case of ALL increased by 30.81%, while the age-standardized incidence rate (ASIR) maintained stable. Subgroup analysis by social-demographic index (SDI) showed that ALL&apos;s ASIR was significantly decreased in high SDI countries, but were moderately increased in high-middle SDI countries. The change trends of age-standardized death rate and DALY rate were similar to ASIR trends. Subgroup analysis by age groups showed that children and the elderly were more likely to suffer ALL. Risk factor analysis demonstrated that smoking was the most significant contributor to ALL&apos;s death and DALY in the globe. Besides, the high body-mass index is playing an increasingly important role in ALL-caused mortality. Multiple methods to counteract potential risk factors should be adopted, such as controlling body-mass index in all regions and avoiding occupational exposure to carcinogens in low SDI countries.
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USP10 deletion inhibits macrophage-derived foam cell formation and cellular-oxidized low density lipoprotein uptake by promoting the degradation of CD36

Xiaohong Xia, Tumei Hu, Jinchan He, Qiong Xu, Cuifu Yu, Xiaolin Liu, Zhenlong Shao, Yuning Liao, Hongbiao Huang, Ningning Liu,

https://doi.org/10.18632/aging.104003 pp 22892—22905

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Xia X, Hu T, He J, Xu Q, Yu C, Liu X, Shao Z, Liao Y, Huang H, Liu N, . USP10 deletion inhibits macrophage-derived foam cell formation and cellular-oxidized low density lipoprotein uptake by promoting the degradation of CD36. . 12:22892-22905. https://doi.org/10.18632/aging.104003

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                TY  - JOUR
                AU  - Xia, Xiaohong 
                AU  - Hu, Tumei 
                AU  - He, Jinchan 
                AU  - Xu, Qiong 
                AU  - Yu, Cuifu 
                AU  - Liu, Xiaolin 
                AU  - Shao, Zhenlong 
                AU  - Liao, Yuning 
                AU  - Huang, Hongbiao 
                AU  - Liu, Ningning 
                TI  - USP10 deletion inhibits macrophage-derived foam cell formation and cellular-oxidized low density lipoprotein uptake by promoting the degradation of CD36
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104003
                DO  - 10.18632/aging.104003
                SP  - 22892
                EP  - 22905
                PY  - 
                AB  - Foam cell formation process is involved in the pathogenesis of atherosclerosis (AS). Activation of this biological process depends on lipid uptake by scavenger receptors, such as CD36, SR-A and SR-B1. Among these receptors, CD36 is the principal one because it dominates roughly 50% lipid uptake in monocytes. In this study, our western blotting and RT-qPCR assays revealed that USP10 inhibition promotes the degradation of CD36 protein but does not change its mRNA level. In addition, Co-IP results showed that USP10 interacts with CD36 and stabilizes CD36 protein by cleaving poly-ubiquitin on CD36. Significantly, USP10 promotes foam cell formation. Immunofluorescence and Oil red O staining assays show that inhibition or knockdown of USP10 suppresses lipid uptake and foam cell formation by macrophages. In conclusion, USP10 promotes the development and progression of atherosclerosis through stabilizing CD36 protein expression. The regulation of USP10-CD36 may provide a significant therapeutic scheme in atherosclerosis.
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Construction of immune-related gene pairs signature to predict the overall survival of osteosarcoma patients

Long-Qing Li, Liang-Hao Zhang, Yan Zhang, Xin-Chang Lu, Yi Zhang, Yong-Kui Liu, Manhas Abdul Khader, Jia-Wen, Tao-Liu, Jia-Zhen Li,

https://doi.org/10.18632/aging.104017 pp 22906—22926

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Li L, Zhang L, Zhang Y, Lu X, Zhang Y, Liu Y, Khader MA, Jia-Wen , Tao-Liu , Li J, . Construction of immune-related gene pairs signature to predict the overall survival of osteosarcoma patients. . 12:22906-22926. https://doi.org/10.18632/aging.104017

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                TY  - JOUR
                AU  - Li, Long-Qing 
                AU  - Zhang, Liang-Hao 
                AU  - Zhang, Yan 
                AU  - Lu, Xin-Chang 
                AU  - Zhang, Yi 
                AU  - Liu, Yong-Kui 
                AU  - Khader, Manhas Abdul 
                AU  - Jia-Wen,  
                AU  - Tao-Liu,  
                AU  - Li, Jia-Zhen 
                TI  - Construction of immune-related gene pairs signature to predict the overall survival of osteosarcoma patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104017
                DO  - 10.18632/aging.104017
                SP  - 22906
                EP  - 22926
                PY  - 
                AB  - The purpose of this study is to establish the prognosis of osteosarcoma patients based on the characteristics of immune-related gene pairs. We used the lasso Cox regression model to construct and verify the signature consisting of 14 immune-related gene pairs. This signature can accurately predict the overall survival of osteosarcoma patients and is an independent prognostic factor for osteosarcoma patients. For this we constructed a signature-based nomogram. The results of the nomogram show that our signature can bring clinical net benefits. We then assessed the abundance of infiltrating immune cells in each sample, and combine the results of the gene set enrichment analysis of a single sample to explore the differences in the immune microenvironment between IRPG signature groups. The result of gene set enrichment analysis shows the strong relationship between signature and immune system. Finally, we evaluated the relationship between signature and immunotherapy efficiency using algorithms such as TIMI and SubMap to explore patients who might benefit from immunotherapy. In conclusion, our signature can predict the overall survival rate of osteosarcoma patients and provide potential guidance for exploring patients who may benefit from immunotherapy.
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Cause of death among patients with colorectal cancer: a population-based study in the United States

Jiayuan Chen, Yongqiang Zheng, Haihong Wang, Dejun Zhang, Lei Zhao, Dandan Yu, Zhenyu Lin, Tao Zhang,

https://doi.org/10.18632/aging.104022 pp 22927—22948

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Chen J, Zheng Y, Wang H, Zhang D, Zhao L, Yu D, Lin Z, Zhang T, . Cause of death among patients with colorectal cancer: a population-based study in the United States. . 12:22927-22948. https://doi.org/10.18632/aging.104022

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                TY  - JOUR
                AU  - Chen, Jiayuan 
                AU  - Zheng, Yongqiang 
                AU  - Wang, Haihong 
                AU  - Zhang, Dejun 
                AU  - Zhao, Lei 
                AU  - Yu, Dandan 
                AU  - Lin, Zhenyu 
                AU  - Zhang, Tao 
                TI  - Cause of death among patients with colorectal cancer: a population-based study in the United States
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104022
                DO  - 10.18632/aging.104022
                SP  - 22927
                EP  - 22948
                PY  - 
                AB  - CRC (Colorectal cancer) is one of the most common causes of death worldwide and in the US (United States). In this study, we aim to perform a population-based analysis on the cause of death among patients with CRC in the US. A total of 834,510 CRC patients diagnosed between 1975 and 2016 in the US were selected from the SEER (Surveillance, Epidemiology, and End Results) program. Causes of death among CRC patients were characterized and SMRs (standardized mortality ratios) of death from non-cancer causes were calculated. Among all CRC patients included in this study, a total of 531,507 deaths were recorded, of which 51.3% were due to CRC, 10.3% were due to other cancers, and 38.4% were due to non-cancer causes. Recently, there has been a relative decrease in index-cancer deaths and an increase in non-cancer causes among CRC patients. The mortality risk from non-cancer rises with accumulating age and longer follow-up time. Cardiovascular diseases are the most prevalent non-cancer causes, accounting for 20.3% of all deaths among CRC patients. Compared with the general population, the mortality rate of non-cancer deaths among CRC patients is doubled (SMR, 2.02; 95% confidence interval, 2.01-2.03).
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In vitro and in vivo efficacy of the novel oral proteasome inhibitor NNU546 in multiple myeloma

Hui Zhou, Meng Lei, Wang Wang, Mengjie Guo, Jia Wang, Haoyang Zhang, Li Qiao, Huayun Feng, Zhaogang Liu, Lijuan Chen, Jianhao Hou, Xueyuan Wang, Chenxi Gu, Bo Zhao, Evgeny Izumchenko, Ye Yang, Yongqiang Zhu,

https://doi.org/10.18632/aging.104023 pp 22949—22974

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Zhou H, Lei M, Wang W, Guo M, Wang J, Zhang H, Qiao L, Feng H, Liu Z, Chen L, Hou J, Wang X, Gu C, et al, . In vitro and in vivo efficacy of the novel oral proteasome inhibitor NNU546 in multiple myeloma. . 12:22949-22974. https://doi.org/10.18632/aging.104023

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Provider: 
 TY - JOUR
 AU - Zhou, Hui 
 AU - Lei, Meng 
 AU - Wang, Wang 
 AU - Guo, Mengjie 
 AU - Wang, Jia 
 AU - Zhang, Haoyang 
 AU - Qiao, Li 
 AU - Feng, Huayun 
 AU - Liu, Zhaogang 
 AU - Chen, Lijuan 
 AU - Hou, Jianhao 
 AU - Wang, Xueyuan 
 AU - Gu, Chenxi 
 AU - Zhao, Bo 
 AU - Izumchenko, Evgeny 
 AU - Yang, Ye 
 AU - Zhu, Yongqiang 
 TI - In vitro and in vivo efficacy of the novel oral proteasome inhibitor NNU546 in multiple myeloma
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104023
 DO - 10.18632/aging.104023
 SP - 22949
 EP - 22974
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Zhou, Hui 
 AU - Lei, Meng 
 AU - Wang, Wang 
 AU - Guo, Mengjie 
 AU - Wang, Jia 
 AU - Zhang, Haoyang 
 AU - Qiao, Li 
 AU - Feng, Huayun 
 AU - Liu, Zhaogang 
 AU - Chen, Lijuan 
 AU - Hou, Jianhao 
 AU - Wang, Xueyuan 
 AU - Gu, Chenxi 
 AU - Zhao, Bo 
 AU - Izumchenko, Evgeny 
 AU - Yang, Ye 
 AU - Zhu, Yongqiang 
 TI - In vitro and in vivo efficacy of the novel oral proteasome inhibitor NNU546 in multiple myeloma
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104023
 DO - 10.18632/aging.104023
 SP - 22949
 EP - 22974
 PY - 
 AB - Proteasome inhibition demonstrates highly effective impact on multiple myeloma (MM) treatment. Here, we aimed to examine anti-tumor efficiency and underlying mechanisms of a novel well tolerated orally applicable proteasome inhibitor NNU546 and its hydrolyzed pharmacologically active form NNU219. NNU219 showed more selective inhibition to proteasome catalytic subunits and less off-target effect than bortezomib ex vivo. Moreover, intravenous and oral administration of either NNU219 or NNU546 led to more sustained pharmacodynamic inhibitions of proteasome activities compared with bortezomib. Importantly, NNU219 exhibited potential anti-MM activity in both MM cell lines and primary samples in vitro. The anti-MM activity of NNU219 was associated with induction of G2/M-phase arrest and apoptosis via activation of the caspase cascade and endoplasmic reticulum stress response. Significant growth-inhibitory effects of NNU219 and NNU546 were observed in 3 different human MM xenograft mouse models. Furthermore, such observation was even found in the presence of a bone marrow microenvironment. Taken together, these findings provided the basis for clinical trial of NNU546 to determine its potential as a candidate for MM treatment.
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Silencing KIF14 reverses acquired resistance to sorafenib in hepatocellular carcinoma

Qiankun Zhu, Haiyang Ren, Xiaodong Li, Bo Qian, Shengjie Fan, Fengli Hu, Lishan Xu, Bo Zhai,

https://doi.org/10.18632/aging.104028 pp 22975—23003

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Zhu Q, Ren H, Li X, Qian B, Fan S, Hu F, Xu L, Zhai B, . Silencing KIF14 reverses acquired resistance to sorafenib in hepatocellular carcinoma. . 12:22975-23003. https://doi.org/10.18632/aging.104028

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Provider: 
 TY - JOUR
 AU - Zhu, Qiankun 
 AU - Ren, Haiyang 
 AU - Li, Xiaodong 
 AU - Qian, Bo 
 AU - Fan, Shengjie 
 AU - Hu, Fengli 
 AU - Xu, Lishan 
 AU - Zhai, Bo 
 TI - Silencing KIF14 reverses acquired resistance to sorafenib in hepatocellular carcinoma
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104028
 DO - 10.18632/aging.104028
 SP - 22975
 EP - 23003
 PY - 
 AB - For nearly a decade, sorafenib has served as a first-line chemotherapeutic drug for the treatment of hepatocellular carcinoma (HCC), but it displays only limited efficacy against advanced drug-resistant HCC. Regorafenib, the first second-line drug approved for treatment after sorafenib failure, can reverse resistance to sorafenib. We used bioinformatics methods to identify genes whose expression was differentially induced by sorafenib and regorafenib in HCC. We identified KIF14 as an oncogene involved in the acquired resistance to sorafenib in HCC and investigated its potential as a target for reversing this resistance. Sustained exposure of resistant HCC cells to sorafenib activated the AKT pathway, which in turn upregulated KIF14 expression by increasing expression of the transcription factor ETS1. Silencing KIF14 reversed the acquired resistance to sorafenib by inhibiting AKT activation and downregulating ETS1 expression by blocking the AKT&#x2013;ETS1&#x2013;KIF14 positive feedback loop. Moreover, injection of siKIF14 with sorafenib suppressed growth of sorafenib-resistant HCC tumors in mice. These results demonstrate that targeting KIF14 could be an effective means of reversing sorafenib failure or strengthening sorafenib&#x2019;s antitumor effects.
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Patrolling monocytes inhibit osteosarcoma metastasis to the lung

Ting Chen, Lin Zhao,

https://doi.org/10.18632/aging.104041 pp 23004—23016

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Chen T, Zhao L, . Patrolling monocytes inhibit osteosarcoma metastasis to the lung. . 12:23004-23016. https://doi.org/10.18632/aging.104041

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                TY  - JOUR
                AU  - Chen, Ting 
                AU  - Zhao, Lin 
                TI  - Patrolling monocytes inhibit osteosarcoma metastasis to the lung
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104041
                DO  - 10.18632/aging.104041
                SP  - 23004
                EP  - 23016
                PY  - 
                AB  - Immune infiltration is associated with osteosarcoma metastasis. However, previous studies have not accounted for the functional diversity of the cells involved in the immune response. We conducted a comprehensive comparative analysis of the tumor-infiltrating immune cells in metastatic and non-metastatic osteosarcoma tissues based on a deconvolution algorithm (CIBERSORT). Twenty-two immune cell subsets were evaluated for their association with the presence or absence of metastasis in osteosarcoma patients. A lack of monocytes was associated with osteosarcoma metastasis; however, the levels of M1 macrophages, M2 macrophages and other immune cell subsets did not differ between the metastatic and non-metastatic groups. Additionally, a higher proportion of monocytes was associated with a better prognosis in osteosarcoma patients. Animal experiments demonstrated that the number of metastatic nodules was higher in mice lacking patrolling monocytes than in control mice. Our data indicated that the cellular composition of the immune infiltrate may subtly differ among osteosarcoma patients, and that patrolling monocytes inhibit osteosarcoma metastasis to the lungs of mice. Thus, the composition of the immune infiltrate and the level of patrolling monocytes may be important determinants of whether metastasis occurs in osteosarcoma patients.
                ER  -

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Autophagy is induced in human keratinocytes during human papillomavirus 11 pseudovirion entry

Rui Han, Chunting Hua, Siyuan Sun, Boya Zhang, Yinjing Song, Stijn van der Veen, Hao Cheng,

https://doi.org/10.18632/aging.104046 pp 23017—23028

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Han R, Hua C, Sun S, Zhang B, Song Y, van der Veen S, Cheng H, . Autophagy is induced in human keratinocytes during human papillomavirus 11 pseudovirion entry. . 12:23017-23028. https://doi.org/10.18632/aging.104046

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                TY  - JOUR
                AU  - Han, Rui 
                AU  - Hua, Chunting 
                AU  - Sun, Siyuan 
                AU  - Zhang, Boya 
                AU  - Song, Yinjing 
                AU  - van der Veen, Stijn 
                AU  - Cheng, Hao 
                TI  - Autophagy is induced in human keratinocytes during human papillomavirus 11 pseudovirion entry
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104046
                DO  - 10.18632/aging.104046
                SP  - 23017
                EP  - 23028
                PY  - 
                AB  - Human papillomavirus type 11 (HPV11) is one of the main causes of condyloma acuminatum, a widespread sexually transmitted disease. During infection of its primary target cell, keratinocytes, it is likely to encounter the autophagy pathway, which is an intracellular maintenance process that is also able to target invading pathogens. It is currently unknown whether HPV11 is targeted by autophagy or whether it is able to escape autophagy-mediated killing. Here, we investigated the autophagy response during HPV11 pseudovirion (PsV) entry in human keratinocytes. Transmission electron microscopy showed that intracellular PsVs were sequestered in lumen of double-membrane autophagosomes that subsequently appeared to fuse with lysosomes, while confocal microscopy showed induction LC3 puncta, the hallmark of induced autophagy activity. Furthermore, quantitative infection assays showed that high autophagy activity resulted in reduced HPV11 PsV infectivity. Therefore, the autophagy pathway seemed to actively target invading HPV11 PsVs for destruction in the autolysosome. Western analysis on the phosphorylation state of autophagy regulators and upstream pathways indicated that autophagy was activated through interplay between Erk and Akt signaling. In conclusion, autophagy functions as a cellular protection mechanism against intracellular HPV11 and therefore therapies that stimulate autophagy may prevent recurrent condyloma acuminatum by helping eliminate latent HPV11 infections.
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ERRα inhibitor acts as a potential agonist of PPARγ to induce cell apoptosis and inhibit cell proliferation in endometrial cancer

Meimei Huang, Lili Chen, Xiaodan Mao, Guifen Liu, Yuqin Gao, Xiaoqing You, Min Gao, Jalid Sehouli, Pengming Sun,

https://doi.org/10.18632/aging.104049 pp 23029—23046

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Huang M, Chen L, Mao X, Liu G, Gao Y, You X, Gao M, Sehouli J, Sun P, . ERRα inhibitor acts as a potential agonist of PPARγ to induce cell apoptosis and inhibit cell proliferation in endometrial cancer. . 12:23029-23046. https://doi.org/10.18632/aging.104049

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                TY  - JOUR
                AU  - Huang, Meimei 
                AU  - Chen, Lili 
                AU  - Mao, Xiaodan 
                AU  - Liu, Guifen 
                AU  - Gao, Yuqin 
                AU  - You, Xiaoqing 
                AU  - Gao, Min 
                AU  - Sehouli, Jalid 
                AU  - Sun, Pengming 
                TI  - ERRα inhibitor acts as a potential agonist of PPARγ to induce cell apoptosis and inhibit cell proliferation in endometrial cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104049
                DO  - 10.18632/aging.104049
                SP  - 23029
                EP  - 23046
                PY  - 
                AB  - Two transcriptional factors, peroxisome proliferator-activated receptor-&#x3B3; (PPAR&#x3B3;) and estrogen-related receptor-&#x3B1; (ERR&#x3B1;), have been reported to be key regulators of cellular energy metabolism. However, the relationship between ERR&#x3B1; and PPAR&#x3B3; in the development of endometrial cancer (EC) is still unclear. The expression levels of PPAR&#x3B3; and ERR&#x3B1; in EC were evaluated by quantitative real-time PCR, western blot, tissue array and immunohistochemistry. A significant negative correlation was identified between PPAR&#x3B3; and ERR&#x3B1; expression in women with EC (&#x3C1;=-0.509, P&lt;0.001). Bioinformatics analyses showed that PPAR&#x3B3; and ERR&#x3B1; can activate or inhibit the same genes involved in cell proliferation and apoptosis through a similar ModFit. ERR&#x3B1; activation or PPAR&#x3B3; inhibition could promote proliferation and inhibit apoptosis through the Bcl-2/Caspase3 pathways. Both PPAR&#x3B3; and ERR&#x3B1; can serve as serum tumor markers. Surprisingly, as evaluated by receiver operating characteristic (ROC) curves and a logistic model, a PPAR&#x3B3;/ERR&#x3B1; ratio&#x2264;1.86 (area under the ROC curve (AUC)=0.915, Youden index=0.6633, P&lt;0.001) was an independent risk factor for endometrial carcinogenesis (OR=14.847, 95% CI= 1.6-137.748, P=0.018). EC patients with PPAR&#x3B3;(-)/ERR&#x3B1;(+) had the worst overall survival and disease-free survival rates (both P&lt;0.001). Thus, a dynamic imbalance between PPAR&#x3B3; and ERR&#x3B1; leads to endometrial carcinogenesis and predicts the EC prognosis.
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Circulating non-coding RNA cluster predicted the tumorigenesis and development of colorectal carcinoma

Jie Li, Yifei Feng, Ding Heng, Ranran Chen, Yong Wang, Ziwei Xu, Dongsheng Zhang, Chuan Zhang, Yue Zhang, Dongjian Ji, Junwei Tang, Yueming Sun,

https://doi.org/10.18632/aging.104055 pp 23047—23066

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Li J, Feng Y, Heng D, Chen R, Wang Y, Xu Z, Zhang D, Zhang C, Zhang Y, Ji D, Tang J, Sun Y, . Circulating non-coding RNA cluster predicted the tumorigenesis and development of colorectal carcinoma. . 12:23047-23066. https://doi.org/10.18632/aging.104055

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                TY  - JOUR
                AU  - Li, Jie 
                AU  - Feng, Yifei 
                AU  - Heng, Ding 
                AU  - Chen, Ranran 
                AU  - Wang, Yong 
                AU  - Xu, Ziwei 
                AU  - Zhang, Dongsheng 
                AU  - Zhang, Chuan 
                AU  - Zhang, Yue 
                AU  - Ji, Dongjian 
                AU  - Tang, Junwei 
                AU  - Sun, Yueming 
                TI  - Circulating non-coding RNA cluster predicted the tumorigenesis and development of colorectal carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104055
                DO  - 10.18632/aging.104055
                SP  - 23047
                EP  - 23066
                PY  - 
                AB  - Carcinoembryonic antigen (CEA) is the most significant plasma biomarker in colorectal cancer (CRC), which is mainly used to diagnose and monitor the recurrence of CRC. However, due to the low sensitivity of CEA, it is more recommended for postoperative surveillance rather than early diagnosis. It is necessary to find efficient biomarkers for CRC. In this study, the expression of plasma non-coding RNAs was confirmed in three independent cohorts with total 1201 participants. First, 12 non-coding RNAs were screened from 9 plasma samples by using microarray. The expression of selected non-coding RNAs was further validated by multiphase detection and risk score analysis. We found that miR-20b-5p, miR-329-3p, miR-374b-5p, miR-503-5p, XLOC_001120 and ENSG00000243766.2 were significantly elevated in CRC plasma, and the AUC in training and validation set was 0.996 and 0.954, respectively. Moreover, miR-20b-5p, miR-329-3p and miR-503-5p were found elevated in plasma from larger tumors (5 cm as the cutoff) in CRC patients, and the merged AUC in training and validation set was 0.896 and 0.881. In conclusion, a panel of 6 non-coding RNAs showed their important clinical value for the early diagnosis of CRC. Among, miR-20b-5p, miR-329-3p and miR-503-5p might be the potential markers for evaluating larger tumor size of CRC.
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CD138^- multiple myeloma cells express high level of CHK1 which correlated to overall survival in MM patient

Dong Wu, Peihua Zhang, Fangmei Li, Ying Shen, Hongli Chen, Yuandong Feng, Aili He, Fangxia Wang,

https://doi.org/10.18632/aging.104066 pp 23067—23081

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Wu D, Zhang P, Li F, Shen Y, Chen H, Feng Y, He A, Wang F, . CD138^- multiple myeloma cells express high level of CHK1 which correlated to overall survival in MM patient. . 12:23067-23081. https://doi.org/10.18632/aging.104066

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Provider: 
 TY - JOUR
 AU - Wu, Dong 
 AU - Zhang, Peihua 
 AU - Li, Fangmei 
 AU - Shen, Ying 
 AU - Chen, Hongli 
 AU - Feng, Yuandong 
 AU - He, Aili 
 AU - Wang, Fangxia 
 TI - CD138- multiple myeloma cells express high level of CHK1 which correlated to overall survival in MM patient
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104066
 DO - 10.18632/aging.104066
 SP - 23067
 EP - 23081
 PY - 
 AB - Multiple myeloma (MM) is a disease in which abnormal plasma cells proliferate and secrete monoclonal immunoglobulin in the bone marrow. The main characteristic of plasma cells is the expression of the cell surface antigen syndecan-1 (CD138). However, the expression of CD138 is limited to terminally differentiated plasma cells during B cell development. A small subpopulation (2~5%) of human MM cells that lack CD138 expression has been shown to possess enormous proliferation potential in vitro experiment and in animal models, and they also can differentiate into CD138+ plasma cells. Thus, this small subset of MM cells was regarded as myeloma cancer stem cell (MCSC). However, its characteristics associated with the pathogenesis of MM remain unclear. In this study, we analyzed the gene expression data of CD138 cell lines downloaded from Gene Expression Omnibus (GEO) database. Limma package in RStudio was used to identify differentially expressed genes (DEGs). Genes enrichment and protein-protein interaction (PPI) network analysis were performed on DAVID and STRING databases. Furthermore, overall survival (OS) analysis in MM patient was utilized to screen out the hub-genes closely associate with the MM pathogenesis process. Hub-genes expression validation and receiver operating characteristic curve (ROC) analysis was performed in different stages of plasma cell disorder diseases. Finally, we verified these findings in MM patient samples. Through integrated bioinformatics analysis of MM CD138- and CD138+ cell lines, we found that CDC7, CDK1, and CHK1 are highly expressed in CD138- MM cells. These genes are crucial in the G2/M phase of the cell cycle pathway, which is closely related to the malignant proliferation in various tumor cells. Of note, we found that patients with high expression of CDC7, CDK1, and CHK1 had shorter overall survival time. The expression of CHK1 was significantly increased in MM cells compared with normal plasma cell (NPC) and MGUS. More importantly, we further clarified that the expression of CHK1 in release/refraction MM (R/R MM) has obviously increased compared with new diagnosed MM (ND MM).
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Deubiquitinase USP7 regulates Drosophila aging through ubiquitination and autophagy

Lang Cui, Wenhao Song, Yao Zeng, Qi Wu, Ziqiang Fan, Tiantian Huang, Bo Zeng, Mingwang Zhang, Qingyong Ni, Yan Li, Tao Wang, Diyan Li, Xueping Mao, Ting Lian, Deying Yang, Mingyao Yang, Xiaolan Fan,

https://doi.org/10.18632/aging.104067 pp 23082—23095

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Cui L, Song W, Zeng Y, Wu Q, Fan Z, Huang T, Zeng B, Zhang M, Ni Q, Li Y, Wang T, Li D, Mao X, et al, . Deubiquitinase USP7 regulates Drosophila aging through ubiquitination and autophagy. . 12:23082-23095. https://doi.org/10.18632/aging.104067

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Provider: 
 TY - JOUR
 AU - Cui, Lang 
 AU - Song, Wenhao 
 AU - Zeng, Yao 
 AU - Wu, Qi 
 AU - Fan, Ziqiang 
 AU - Huang, Tiantian 
 AU - Zeng, Bo 
 AU - Zhang, Mingwang 
 AU - Ni, Qingyong 
 AU - Li, Yan 
 AU - Wang, Tao 
 AU - Li, Diyan 
 AU - Mao, Xueping 
 AU - Lian, Ting 
 AU - Yang, Deying 
 AU - Yang, Mingyao 
 AU - Fan, Xiaolan 
 TI - Deubiquitinase USP7 regulates Drosophila aging through ubiquitination and autophagy
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104067
 DO - 10.18632/aging.104067
 SP - 23082
 EP - 23095
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Cui, Lang 
 AU - Song, Wenhao 
 AU - Zeng, Yao 
 AU - Wu, Qi 
 AU - Fan, Ziqiang 
 AU - Huang, Tiantian 
 AU - Zeng, Bo 
 AU - Zhang, Mingwang 
 AU - Ni, Qingyong 
 AU - Li, Yan 
 AU - Wang, Tao 
 AU - Li, Diyan 
 AU - Mao, Xueping 
 AU - Lian, Ting 
 AU - Yang, Deying 
 AU - Yang, Mingyao 
 AU - Fan, Xiaolan 
 TI - Deubiquitinase USP7 regulates Drosophila aging through ubiquitination and autophagy
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104067
 DO - 10.18632/aging.104067
 SP - 23082
 EP - 23095
 PY - 
 AB - Ubiquitination-mediated protein degradation is the selective degradation of diverse forms of damaged proteins that are tagged with ubiquitin, while deubiquitinating enzymes reverse ubiquitination-mediated protein degradation by removing the ubiquitin chain from the target protein. The interactions of ubiquitinating and deubiquitinating enzymes are required to maintain protein homeostasis. The ubiquitin-specific protease USP7 is a deubiquitinating enzyme that indirectly plays a role in repairing DNA damage and development. However, the mechanism of its participation in aging has not been fully explored. Regarding this issue, we found that USP7 was necessary to maintain the normal lifespan of Drosophila melanogaster, and knockdown of dusp7 shortened the lifespan and reduced the ability of Drosophila to cope with starvation, oxidative stress and heat stress. Furthermore, we showed that the ability of USP7 to regulate aging depends on the autophagy and ubiquitin signaling pathways. Furthermore, 2,5-dimethyl-celecoxib (DMC), a derivative of celecoxib, can partially restore the shortened lifespan and aberrant phenotypes caused by dusp7 knockdown. Our results suggest that USP7 is an important factor involved in the regulation of aging, and related components in this regulatory pathway may become new targets for anti-aging treatments.
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Protective effect of DLX6-AS1 silencing against cerebral ischemia/reperfusion induced impairments

Xiamin Hu, Zifei Xiang, Wei Zhang, Zhijun Yu, Xiaoming Xin, Rong Zhang, Youping Deng, Qiong Yuan,

https://doi.org/10.18632/aging.104070 pp 23096—23113

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Hu X, Xiang Z, Zhang W, Yu Z, Xin X, Zhang R, Deng Y, Yuan Q, . Protective effect of DLX6-AS1 silencing against cerebral ischemia/reperfusion induced impairments. . 12:23096-23113. https://doi.org/10.18632/aging.104070

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                TY  - JOUR
                AU  - Hu, Xiamin 
                AU  - Xiang, Zifei 
                AU  - Zhang, Wei 
                AU  - Yu, Zhijun 
                AU  - Xin, Xiaoming 
                AU  - Zhang, Rong 
                AU  - Deng, Youping 
                AU  - Yuan, Qiong 
                TI  - Protective effect of DLX6-AS1 silencing against cerebral ischemia/reperfusion induced impairments
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104070
                DO  - 10.18632/aging.104070
                SP  - 23096
                EP  - 23113
                PY  - 
                AB  - In the present study, we investigated the role of lncRNA mus distal-less homeobox 6 antisense 1 (DLX6-AS1) during cerebral impairment induced by stroke. DLX6-AS1 levels were upregulated during ischemia/reperfusion (I/R) and downregulation of DLX6-AS1 reduced acute injury and ameliorated long-term neurological impairments induced by cerebral I/R in mice. Additionally, silencing of DLX6-AS1 significantly decreased the neuronal apoptosis in vivo and in vitro. Furthermore, inhibition of miRNA-149-3p led to enhance the apoptosis, which confirmed that DLX6-AS1 could sponge miR-149-3p. Finally, BOK was predicted to be the target of miR-149-3p using TargetScanVert software. And the silencing of DLX6-AS1 inhibited BOK expression both in vivo and in vitro, which was reversed by a miR-149-3p inhibitor. At meantime, BOK promoted OGD/R induced apoptosis in N2a cells. Therefore, this suggests that miR-149-3p sponging by DLX6-AS1 may lead to cerebral neuron I/R-induced impairments through upregulation of apoptotic BOK activity, which offers a new approach to the treatment of stroke impairment.
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Intracellular and extracellular S100A9 trigger epithelial-mesenchymal transition and promote the invasive phenotype of pituitary adenoma through activation of AKT1

Ning Huang, Guanjian Zhao, Qiang Yang, Jiahe Tan, Ying Tan, Jiqin Zhang, Yuan Cheng, Jin Chen,

https://doi.org/10.18632/aging.104072 pp 23114—23128

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Huang N, Zhao G, Yang Q, Tan J, Tan Y, Zhang J, Cheng Y, Chen J, . Intracellular and extracellular S100A9 trigger epithelial-mesenchymal transition and promote the invasive phenotype of pituitary adenoma through activation of AKT1. . 12:23114-23128. https://doi.org/10.18632/aging.104072

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                TY  - JOUR
                AU  - Huang, Ning 
                AU  - Zhao, Guanjian 
                AU  - Yang, Qiang 
                AU  - Tan, Jiahe 
                AU  - Tan, Ying 
                AU  - Zhang, Jiqin 
                AU  - Cheng, Yuan 
                AU  - Chen, Jin 
                TI  - Intracellular and extracellular S100A9 trigger epithelial-mesenchymal transition and promote the invasive phenotype of pituitary adenoma through activation of AKT1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104072
                DO  - 10.18632/aging.104072
                SP  - 23114
                EP  - 23128
                PY  - 
                AB  - Pituitary adenoma (PA) is mostly benign intracranial tumor, but it also displays invasive growth characteristics and provokes challenging clinical conditions. S100A9 protein enhances tumor progression. In this study, we firstly demonstrated that both intracellular and extracellular S100A9 promoted the expression of Vimentin and Intercellular cell adhesion molecule-1 (ICAM-1), coupled with reduced E-cadherin in PA. As a result, PA acquired the phenotype of Epithelial-Mesenchymal Transition (EMT), leading to proliferation, cell cycle progression, migration and invasion. In addition, we indicated S100A9-induced EMT was mediated by activation of AKT1. Furthermore, immunohistochemistry showed that S100A9 expression was higher in invasive PA than that in non-invasive PA. These data extended our understanding for the effects of S100A9 on PA invasion and contributed to further development of a promising therapeutic target for invasive PA.
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Cognitive frailty in relation to adverse health outcomes independent of multimorbidity: results from the China health and retirement longitudinal study

Chen Chen, JuYoung Park, Chenkai Wu, QianLi Xue, George Agogo, Ling Han, Emiel O. Hoogendijk, Zuyun Liu, Zunyou Wu,

https://doi.org/10.18632/aging.104078 pp 23129—23145

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Chen C, Park J, Wu C, Xue Q, Agogo G, Han L, Hoogendijk EO, Liu Z, Wu Z, . Cognitive frailty in relation to adverse health outcomes independent of multimorbidity: results from the China health and retirement longitudinal study. . 12:23129-23145. https://doi.org/10.18632/aging.104078

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                TY  - JOUR
                AU  - Chen, Chen 
                AU  - Park, JuYoung 
                AU  - Wu, Chenkai 
                AU  - Xue, QianLi 
                AU  - Agogo, George 
                AU  - Han, Ling 
                AU  - Hoogendijk, Emiel O. 
                AU  - Liu, Zuyun 
                AU  - Wu, Zunyou 
                TI  - Cognitive frailty in relation to adverse health outcomes independent of multimorbidity: results from the China health and retirement longitudinal study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104078
                DO  - 10.18632/aging.104078
                SP  - 23129
                EP  - 23145
                PY  - 
                AB  - Our objectives were to evaluate: 1) the associations of cognitive frailty with various health outcomes including disability, hospitalization, and death; 2) whether the associations differed by multimorbidity. We included data of 5113 Chinese older adults (aged 60+ years) who had baseline cognition and physical frailty assessments (2011 wave) and follow-up for 4 years. About 16.0% (n=820) had cognitive impairment; 6.7% (n=342) had physical frailty; and 1.6% (n=82) met criteria for cognitive frailty. Both cognitive impairment (odds ratios (ORs) range: 1.41 to 2.11) and physical frailty (ORs range: 1.51 to 2.43) were independently associated with basic activities of daily living (BADL), instrumental ADL (IADL), mobility disability, hospitalization, and death among participants without that corresponding outcome at baseline, even after accounting for covariates. Relative to participants who had normal cognition and were nonfrail, those with cognitive frailty had the highest risk for IADL disability (OR=3.40, 95% CI, 1.23&#x2013;9.40) and death (OR=3.89, 95% CI, 2.25&#x2013;6.47). We did not find significant interaction effects between cognitive frailty and multimorbidity (Pinteractions&gt;0.05). Overall, cognitive frailty was associated with disability and death, independent of multimorbidity. This highlights the importance of assessing cognitive frailty in the community to promote primary and secondary preventions for healthy aging.
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pSynGAP1 disturbance-mediated hippocampal oscillation network impairment might contribute to long-term neurobehavioral abnormities in sepsis survivors

Yong Wang, Hua Wei, Jianhua Tong, Muhuo Ji, Jianjun Yang,

https://doi.org/10.18632/aging.104080 pp 23146—23164

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Wang Y, Wei H, Tong J, Ji M, Yang J, . pSynGAP1 disturbance-mediated hippocampal oscillation network impairment might contribute to long-term neurobehavioral abnormities in sepsis survivors. . 12:23146-23164. https://doi.org/10.18632/aging.104080

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                TY  - JOUR
                AU  - Wang, Yong 
                AU  - Wei, Hua 
                AU  - Tong, Jianhua 
                AU  - Ji, Muhuo 
                AU  - Yang, Jianjun 
                TI  - pSynGAP1 disturbance-mediated hippocampal oscillation network impairment might contribute to long-term neurobehavioral abnormities in sepsis survivors
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104080
                DO  - 10.18632/aging.104080
                SP  - 23146
                EP  - 23164
                PY  - 
                AB  - Although more patients survive sepsis and are increasingly discharged from the hospital, they often experience long-term cognitive and psychological impairment with significant socioeconomic impact. However, the pathophysiological mechanisms have not been fully elucidated. In the present study, we showed that LPS induced long-term neurobehavioral abnormities, as reflected by significantly decreased freezing time to context and sucrose preference. Using a high-throughput quantitative proteomic screen, we showed that phosphorylation of synaptic GTPase-activating protein 1 (pSynGAP1) was identified as the hub of synaptic plasticity and was significantly decreased following LPS exposure. This decreased pSynGAP was associated with significantly lower theta and gamma oscillations in the CA1 of the hippocampus. Notably, restoration of pSynGAP1 by roscovitine was able to reverse most of these abnormities. Taken together, our study suggested that pSynGAP1 disturbance-mediated hippocampal oscillation network impairment might play a critical role in long-term neurobehavioral abnormities of sepsis survivors.
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An eleven metabolic gene signature-based prognostic model for clear cell renal cell carcinoma

Yue Wu, Xian Wei, Huan Feng, Bintao Hu, Bo Liu, Yang Luan, Yajun Ruan, Xiaming Liu, Zhuo Liu, Shaogang Wang, Jihong Liu, Tao Wang,

https://doi.org/10.18632/aging.104088 pp 23165—23186

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Wu Y, Wei X, Feng H, Hu B, Liu B, Luan Y, Ruan Y, Liu X, Liu Z, Wang S, Liu J, Wang T, . An eleven metabolic gene signature-based prognostic model for clear cell renal cell carcinoma. . 12:23165-23186. https://doi.org/10.18632/aging.104088

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                TY  - JOUR
                AU  - Wu, Yue 
                AU  - Wei, Xian 
                AU  - Feng, Huan 
                AU  - Hu, Bintao 
                AU  - Liu, Bo 
                AU  - Luan, Yang 
                AU  - Ruan, Yajun 
                AU  - Liu, Xiaming 
                AU  - Liu, Zhuo 
                AU  - Wang, Shaogang 
                AU  - Liu, Jihong 
                AU  - Wang, Tao 
                TI  - An eleven metabolic gene signature-based prognostic model for clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104088
                DO  - 10.18632/aging.104088
                SP  - 23165
                EP  - 23186
                PY  - 
                AB  - In this study, we performed bioinformatics and statistical analyses to investigate the prognostic significance of metabolic genes in clear cell renal cell carcinoma (ccRCC) using the transcriptome data of 539 ccRCC and 72 normal renal tissues from TCGA database. We identified 79 upregulated and 45 downregulated (n=124) metabolic genes in ccRCC tissues. Eleven prognostic metabolic genes (NOS1, ALAD, ALDH3B2, ACADM, ITPKA, IMPDH1, SCD5, FADS2, ACHE, CA4, and HK3) were identified by further analysis. We then constructed an 11-metabolic gene signature-based prognostic risk score model and classified ccRCC patients into high- and low-risk groups. Overall survival (OS) among the high-risk ccRCC patients was significantly shorter than among the low-risk ccRCC patients. Receiver operating characteristic (ROC) curve analysis of the prognostic risk score model showed that the areas under the ROC curve for the 1-, 3-, and 5-year OS were 0.810, 0.738, and 0.771, respectively. Thus, our prognostic model showed favorable predictive power in the TCGA and E-MTAB-1980 ccRCC patient cohorts. We also established a nomogram based on these eleven metabolic genes and validated internally in the TCGA cohort, showing an accurate prediction for prognosis in ccRCC.
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Identification and characterization of dynamically regulated hepatitis-related genes in a concanavalin A-induced liver injury model

Anna Chen, Yidong Wang, Jiaqi Wu, Dong Tang, Qianru Zhu, Anqian Lu, Jin Yang, Zhejun Cai, Junping Shi,

https://doi.org/10.18632/aging.104089 pp 23187—23199

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Chen A, Wang Y, Wu J, Tang D, Zhu Q, Lu A, Yang J, Cai Z, Shi J, . Identification and characterization of dynamically regulated hepatitis-related genes in a concanavalin A-induced liver injury model. . 12:23187-23199. https://doi.org/10.18632/aging.104089

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                TY  - JOUR
                AU  - Chen, Anna 
                AU  - Wang, Yidong 
                AU  - Wu, Jiaqi 
                AU  - Tang, Dong 
                AU  - Zhu, Qianru 
                AU  - Lu, Anqian 
                AU  - Yang, Jin 
                AU  - Cai, Zhejun 
                AU  - Shi, Junping 
                TI  - Identification and characterization of dynamically regulated hepatitis-related genes in a concanavalin A-induced liver injury model
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104089
                DO  - 10.18632/aging.104089
                SP  - 23187
                EP  - 23199
                PY  - 
                AB  - Background: Concanavalin A (ConA)-induced liver damage of mice is a well-established murine model mimicking the human autoimmune hepatitis (AIH). However, the pathogenic genes of the liver injury remain to be revealed.
                Methods: Using time-series liver transcriptome, top dynamic genes were inferred from a set of segmented regression models, and cross-checked by weighted correlation network analysis (WGCNA). AIH murine models created by ConA were used to verify the in vivo effect of these genes.
                Results: We identified 115 top dynamic genes, of which most were overlapped with the hub genes determined by WGCNA. The expression of several top dynamic genes including Cd63, Saa3, Slc10a1, Nrxn1, Ugt2a3, were verified in vivo. Further, Cluster determinant 63 (Cd63) knockdown in mice treated with ConA showed significantly less liver pathology and inflammation as well as higher survival rates than the corresponding controls.
                Conclusion: We have identified the top dynamic genes related to the process of acute liver injury, and highlighted a targeted strategy for Cd63 might have utility for the protection of hepatocellular damage.
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Development and validation of a nomogram with an epigenetic signature for predicting survival in patients with lung adenocarcinoma

Jiao Wang, Li He, Yunliang Tang, Dan Li, Yuting Yang, Zhenguo Zeng,

https://doi.org/10.18632/aging.104090 pp 23200—23216

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Wang J, He L, Tang Y, Li D, Yang Y, Zeng Z, . Development and validation of a nomogram with an epigenetic signature for predicting survival in patients with lung adenocarcinoma. . 12:23200-23216. https://doi.org/10.18632/aging.104090

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                TY  - JOUR
                AU  - Wang, Jiao 
                AU  - He, Li 
                AU  - Tang, Yunliang 
                AU  - Li, Dan 
                AU  - Yang, Yuting 
                AU  - Zeng, Zhenguo 
                TI  - Development and validation of a nomogram with an epigenetic signature for predicting survival in patients with lung adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104090
                DO  - 10.18632/aging.104090
                SP  - 23200
                EP  - 23216
                PY  - 
                AB  - Epigenetic factors play crucial roles in carcinogenesis by modifying chromatin architecture. Here, we established an epigenetic biosignature-based model for examining survival in patients with lung adenocarcinoma (LUAD). We retrieved gene-expression profiles and clinical data from The Cancer Genome Atlas and Gene Expression Omnibus and clustered the data into training (n = 490) and Validation (n = 226) datasets, respectively. To establish an epigenetic model, we identified prognostic epigenetic regulation-related genes by LASSO and Cox regression analyses, and established a novel 11-gene signature, including EPC1, GADD45A, HCFC2, RCOR1, SMARCAL1, TLE2, TRIM28, and ZNF516, for predicting LUAD overall survival (OS). The biosignature performed optimally in both the training and validation sets according to receiver operating characteristic and calibration plots. Moreover, the biosignature classified patients into high- and low-risk clusters with distinct survival times, with Cox regression analysis revealing the biosignature as an independent LUAD prognostic index. Furthermore, the generated nomogram integrating the prognostic gene biosignature and clinical indices predicted LUAD OS with high efficiency and outperformed tumor-node-metastasis staging in LUAD survival prediction. These results demonstrated the efficacy of the epigenetic signature prognostic nomogram for reliably predicting LUAD OS and its potential application for informing clinical decision making and individualized treatment.
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Alteration of tumor-associated macrophage subtypes mediated by KRT6A in pancreatic ductal adenocarcinoma

Junfeng Zhang, Hui Sun, Songsong Liu, Wenjie Huang, Jianyou Gu, Zhiping Zhao, Huan Qin, Liwen Luo, Jiali Yang, Yongfei Fang, Jiayun Ge, Bing Ni, Huaizhi Wang,

https://doi.org/10.18632/aging.104091 pp 23217—23232

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Zhang J, Sun H, Liu S, Huang W, Gu J, Zhao Z, Qin H, Luo L, Yang J, Fang Y, Ge J, Ni B, Wang H, . Alteration of tumor-associated macrophage subtypes mediated by KRT6A in pancreatic ductal adenocarcinoma. . 12:23217-23232. https://doi.org/10.18632/aging.104091

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                TY  - JOUR
                AU  - Zhang, Junfeng 
                AU  - Sun, Hui 
                AU  - Liu, Songsong 
                AU  - Huang, Wenjie 
                AU  - Gu, Jianyou 
                AU  - Zhao, Zhiping 
                AU  - Qin, Huan 
                AU  - Luo, Liwen 
                AU  - Yang, Jiali 
                AU  - Fang, Yongfei 
                AU  - Ge, Jiayun 
                AU  - Ni, Bing 
                AU  - Wang, Huaizhi 
                TI  - Alteration of tumor-associated macrophage subtypes mediated by KRT6A in pancreatic ductal adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104091
                DO  - 10.18632/aging.104091
                SP  - 23217
                EP  - 23232
                PY  - 
                AB  - Pancreatic ductal adenocarcinoma (PDAC) is severely affecting the health and lives of patients. Clarifying the composition and regulatory factors of tumor immune microenvironment (TIME) is helpful for the treatment of PDAC. We analyzed the unique TIMEs and gene expression patterns between PDAC and adjacent normal tissue (ANT) using Gene Expression Omnibus (GEO) to find new immunotherapy targets. The Cancer Genome Atlas (TCGA) datasets were used to elucidate the possible mechanism of which tumor-associated macrophages (TAMs) changed in PDAC. We found that the composition of TAMs subtypes, including M0, M1, and M2, was different between PDAC and ANT, which was validated in recently published single-cell RNA-seq data. Many immune cells interacted with each other to affect the TIME. There were many DEGs enriched in some pathways that could potentially change the immune cell composition. KRT6A was found to be a DEG between PDAC and ANT that overlapped with DEGs between the M0-high group and the M0-low group in TCGA datasets, and it might alter and regulate TAMs via a collection of genes including COL5A2, COL1A2, MIR3606, SPARC, and COL6A3. TAMs, which could be a target of immunotherapy, might be influenced by genes through KRT6A and indicate an undesirable prognosis in PDAC.
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NEAT1 regulates microtubule stabilization via FZD3/GSK3β/P-tau pathway in SH-SY5Y cells and APP/PS1 mice

Yiwan Zhao, Ziqiang Wang, Yunhao Mao, Bing Li, Yuanchang Zhu, Shikuan Zhang, Songmao Wang, Yuyang Jiang, Naihan Xu, Yizhen Xie, Weidong Xie, Yaou Zhang,

https://doi.org/10.18632/aging.104098 pp 23233—23250

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Zhao Y, Wang Z, Mao Y, Li B, Zhu Y, Zhang S, Wang S, Jiang Y, Xu N, Xie Y, Xie W, Zhang Y, . NEAT1 regulates microtubule stabilization via FZD3/GSK3β/P-tau pathway in SH-SY5Y cells and APP/PS1 mice. . 12:23233-23250. https://doi.org/10.18632/aging.104098

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                TY  - JOUR
                AU  - Zhao, Yiwan 
                AU  - Wang, Ziqiang 
                AU  - Mao, Yunhao 
                AU  - Li, Bing 
                AU  - Zhu, Yuanchang 
                AU  - Zhang, Shikuan 
                AU  - Wang, Songmao 
                AU  - Jiang, Yuyang 
                AU  - Xu, Naihan 
                AU  - Xie, Yizhen 
                AU  - Xie, Weidong 
                AU  - Zhang, Yaou 
                TI  - NEAT1 regulates microtubule stabilization via FZD3/GSK3β/P-tau pathway in SH-SY5Y cells and APP/PS1 mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104098
                DO  - 10.18632/aging.104098
                SP  - 23233
                EP  - 23250
                PY  - 
                AB  - Nuclear paraspeckles assembly transcript 1 (NEAT1) is a well-known long noncoding RNA (lncRNA) with various functions in different physiological and pathological processes. Notably, aberrant NEAT1 expression is implicated in the pathogenesis of various neurodegenerative diseases, including Alzheimer&#x2019;s disease (AD). However, the molecular mechanism of NEAT1 in AD remains poorly understood. In this study, we investigated that NEAT1 regulated microtubules (MTs) polymerization via FZD3/GSK3&#x3B2;/p-tau pathway. Downregulation of NEAT1 inhibited Frizzled Class Receptor 3 (FZD3) transcription activity by suppressing H3K27 acetylation (H3K27Ac) at the FZD3 promoter. Our data also demonstrated that P300, an important histone acetyltransferases (HAT), recruited by NEAT1 to bind to FZD3 promoter and mediated its transcription via regulating histone acetylation. In addition, according to immunofluorescence staining of MTs, metformin, a medicine for the treatment of diabetes mellitus, rescued the reduced length of neurites detected in NEAT1 silencing cells. We suspected that metformin may play a neuroprotective role in early AD by increasing NEAT1 expression and through FZD3/GSK3&#x3B2;/p-tau pathway. Collectively, NEAT1 regulates microtubule stabilization via FZD3/GSK3&#x3B2;/P-tau pathway and influences FZD3 transcription activity in the epigenetic way.
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Comprehensive circular RNA expression profiling constructs a ceRNA network and identifies hsa_circ_0000673 as a novel oncogene in distal cholangiocarcinoma

Xin Zhao, Xinxue Zhang, Zhigang Zhang, Zhe Liu, Jiqiao Zhu, Shaocheng Lyu, Lixin Li, Ren Lang, Qiang He,

https://doi.org/10.18632/aging.104099 pp 23251—23274

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Zhao X, Zhang X, Zhang Z, Liu Z, Zhu J, Lyu S, Li L, Lang R, He Q, . Comprehensive circular RNA expression profiling constructs a ceRNA network and identifies hsa_circ_0000673 as a novel oncogene in distal cholangiocarcinoma. . 12:23251-23274. https://doi.org/10.18632/aging.104099

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                TY  - JOUR
                AU  - Zhao, Xin 
                AU  - Zhang, Xinxue 
                AU  - Zhang, Zhigang 
                AU  - Liu, Zhe 
                AU  - Zhu, Jiqiao 
                AU  - Lyu, Shaocheng 
                AU  - Li, Lixin 
                AU  - Lang, Ren 
                AU  - He, Qiang 
                TI  - Comprehensive circular RNA expression profiling constructs a ceRNA network and identifies hsa_circ_0000673 as a novel oncogene in distal cholangiocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104099
                DO  - 10.18632/aging.104099
                SP  - 23251
                EP  - 23274
                PY  - 
                AB  - Circular RNAs (circRNAs) play an important role in cholangiocarcinoma (CCA) development; however, the expression and functions of circRNAs in distal CCA (dCCA) remain unknown. Herein, we explored the expression profile of circRNAs in six paired dCCA tumor and adjacent normal tissue samples using microarray. A total of 171 differentially expressed (DE) circRNAs were identified in dCCA tissues. Host genes of DE circRNAs were enriched in the cellular cytoskeleton and adheren junction. Bioinformatics analyses were used to establish a circRNA-microRNA-mRNA network for dCCA. Protein-protein interaction networks were constructed, and five hub genes were associated with the regulation of the cell cycle based on gene set enrichment analyses. Five DE circRNAs were validated with qRT-PCR in 40 pairs of dCCA tissues, and hsa_circ_0000673 showed promising diagnostic performance in distinguishing dCCA from normal tissues (AUC = 0.85, p &lt; 0.01). Overexpression of hsa_circ_0000673 was associated with tumor invasion (p = 0.001), poor differentiation (p = 0.041), and residual tumor (p = 0.044). In vitro experiments indicated that inhibition of hsa_circ_0000673 suppressed the proliferation, migration, and invasion of CCA cells. This research provided a landscape of dysregulated circRNAs in dCCA and identified hsa_circ_0000673 as a potential biomarker and therapeutic target for dCCA.
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Transcriptome profiling reveals an integrated mRNA–lncRNA signature with predictive value for long-term survival in diffuse large B-cell lymphoma

Qian Gao, Zhiyao Li, Lingxian Meng, Jinsha Ma, Yanfeng Xi, Tong Wang,

https://doi.org/10.18632/aging.104100 pp 23275—23295

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Gao Q, Li Z, Meng L, Ma J, Xi Y, Wang T, . Transcriptome profiling reveals an integrated mRNA–lncRNA signature with predictive value for long-term survival in diffuse large B-cell lymphoma. . 12:23275-23295. https://doi.org/10.18632/aging.104100

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                TY  - JOUR
                AU  - Gao, Qian 
                AU  - Li, Zhiyao 
                AU  - Meng, Lingxian 
                AU  - Ma, Jinsha 
                AU  - Xi, Yanfeng 
                AU  - Wang, Tong 
                TI  - Transcriptome profiling reveals an integrated mRNA–lncRNA signature with predictive value for long-term survival in diffuse large B-cell lymphoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104100
                DO  - 10.18632/aging.104100
                SP  - 23275
                EP  - 23295
                PY  - 
                AB  - For patients with diffuse large B-cell lymphoma (DLBCL), survival at 24 months is a milestone for long-term survival. The purpose of this study was to develop a multigene risk score (MGRS) to refine the International Prognostic Index (IPI) model to identify patients with DLBCL at high risk of death within 24 months. Using a robust statistical strategy, we built a MGRS incorporating nine mRNAs and two lncRNAs. Stratification and multivariable Cox regression analysis confirmed the MGRS as an independent risk factor. A nomogram based on IPI+MGRS model was constructed and its calibration plot showed close agreement between predicted 2-year survival rate and observed rate. The 2-year AUC was bigger with the IPI+MGRS model (&#x394;AUC=0.162; 95%CI 0.1295&#x2013;0.1903) than with the IPI model, and the IPI+MGRS model more accurately predicted the prognostic risk of DLBCL. The 2-year survival decision curve revealed the IPI+MGRS model was more useful clinically than the IPI model. Functional enrichment analysis showed that the MGRS correlated with cell cycle, DNA replication and repair. The results were validated using an independent external dataset. In conclusion, we successfully developed an integrated mRNA&#x2013;lncRNA signature to refine the IPI model for predicting long-term survival of patients with DLBCL.
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Inverse association between periumbilical fat and longevity mediated by complement C3 and cardiac structure

Shihui Fu, Yao Yao, Shengzheng Wu, Juelin Deng, Faqin Lv, Yali Zhao,

https://doi.org/10.18632/aging.104113 pp 23296—23305

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Fu S, Yao Y, Wu S, Deng J, Lv F, Zhao Y, . Inverse association between periumbilical fat and longevity mediated by complement C3 and cardiac structure. . 12:23296-23305. https://doi.org/10.18632/aging.104113

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                TY  - JOUR
                AU  - Fu, Shihui 
                AU  - Yao, Yao 
                AU  - Wu, Shengzheng 
                AU  - Deng, Juelin 
                AU  - Lv, Faqin 
                AU  - Zhao, Yali 
                TI  - Inverse association between periumbilical fat and longevity mediated by complement C3 and cardiac structure
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104113
                DO  - 10.18632/aging.104113
                SP  - 23296
                EP  - 23305
                PY  - 
                AB  - Although abdominal obesity plays a fundamental role in the onset of immune and inflammatory reactions leading to cardiac abnormalities and premature mortality, the potential association between periumbilical fat and longevity mediated by the antibody-complement system and/or cardiac structure and function remains unclear. To address this issue, we collected biochemical and morphological data from 419 centenarians and 491 non-centenarian oldest-old individuals from the China Hainan Centenarian Cohort Study. Centenarians had lower waist circumference (WC), periumbilical fat thickness (PFT), serum complement C3 level, right atrium end-systolic diameter (RAESD), left atrium end-systolic diameter (LAESD), and left ventricular end-diastolic diameter (LVEDD) than non-centenarians (P&lt;0.05 for all comparisons). WC, PFT, complement C3 levels, RAESD, LAESD, and LVEDD were inversely associated with centenarians (P&lt;0.05 for all variables). Complement C3 level, LAESD, and LVEDD were positively associated with PFT and WC (P&lt;0.05 for all variables). RAESD was positively associated with WC and complement C3 level (P&lt;0.05 for both variables). Centenarians had less periumbilical fat, a weaker complement system, and smaller cardiac structure than non-centenarians. Importantly, periumbilical fat was inversely associated with longevity mediated by complement C3 and cardiac structure. This study suggests that successful aging can be promoted by increased efforts to prevent abdominal obesity.
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Identification of immune-related LncRNA for predicting prognosis and immunotherapeutic response in bladder cancer

Yucai Wu, Lei Zhang, Shiming He, Bao Guan, Anbang He, Kunlin Yang, Yanqing Gong, Xuesong Li, Liqun Zhou,

https://doi.org/10.18632/aging.104115 pp 23306—23325

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Wu Y, Zhang L, He S, Guan B, He A, Yang K, Gong Y, Li X, Zhou L, . Identification of immune-related LncRNA for predicting prognosis and immunotherapeutic response in bladder cancer. . 12:23306-23325. https://doi.org/10.18632/aging.104115

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                TY  - JOUR
                AU  - Wu, Yucai 
                AU  - Zhang, Lei 
                AU  - He, Shiming 
                AU  - Guan, Bao 
                AU  - He, Anbang 
                AU  - Yang, Kunlin 
                AU  - Gong, Yanqing 
                AU  - Li, Xuesong 
                AU  - Zhou, Liqun 
                TI  - Identification of immune-related LncRNA for predicting prognosis and immunotherapeutic response in bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104115
                DO  - 10.18632/aging.104115
                SP  - 23306
                EP  - 23325
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) have multiple functions in the cancer immunity response and the tumor microenvironment. To investigate the immune-related lncRNA (IRlncRNA) signature for predicting prognosis and immunotherapeutic response in bladder cancer (BLCA), we extracted BLCA data from The Cancer Genome Atlas (TCGA) database. Finally, a total of 405 cases were enrolled and 8 prognostic IRlncRNAs (MIR181A2HG, AC114730.3, LINC00892, PTPRD-AS1, LINC01013, MRPL23-AS1, LINC01395, AC002454.1) were identified in the training set. Risk scores were calculated to divide patients into high-risk and low-risk groups, and the high-risk patients tended to have a poor overall survival (OS). Multivariate Cox regression analysis confirmed that the IRlncRNA signature could be an independent prognostic factor. The results were subsequently confirmed in the validating set. Additionally, this 8-IRlncRNA classifier was related to recurrence free survival (RFS) of BLCA. Functional characterization revealed this signature mediated immune-related phenotype. This signature was also associated with immune cell infiltration (i.e., macrophages M0, M2, Tregs, CD8 T cells, and neutrophils) and immune checkpoint inhibitors (ICIs) immunotherapy-related biomarkers [mismatch repair (MMR) genes, tumor mutation burden (TMB) and immune checkpoint genes]. The present study highlighted the value of the 8-IRlncRNA signature as a predictor of prognosis and immunotherapeutic response in BLCA.
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The DLG1-AS1/miR-497/YAP1 axis regulates papillary thyroid cancer progression

Yong Huang, KeWei Zhang, Yinghua Li, Yuyin Dai, Hongguang Zhao,

https://doi.org/10.18632/aging.104121 pp 23326—23336

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Huang Y, Zhang K, Li Y, Dai Y, Zhao H, . The DLG1-AS1/miR-497/YAP1 axis regulates papillary thyroid cancer progression. . 12:23326-23336. https://doi.org/10.18632/aging.104121

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                TY  - JOUR
                AU  - Huang, Yong 
                AU  - Zhang, KeWei 
                AU  - Li, Yinghua 
                AU  - Dai, Yuyin 
                AU  - Zhao, Hongguang 
                TI  - The DLG1-AS1/miR-497/YAP1 axis regulates papillary thyroid cancer progression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104121
                DO  - 10.18632/aging.104121
                SP  - 23326
                EP  - 23336
                PY  - 
                AB  - The long non-coding RNA (lncRNA), DLG1-AS1, is upregulated in papillary thyroid cancer (PTC) tissues and cell lines. Here, we found that increased expression of DLG1-AS1 caused lymph node metastasis and advanced tumor-node-metastasis (TNM) stage. DLG1-AS1 knockdown inhibited proliferation, invasion, and migration of PTC cells, and impaired tumorigenesis in vivo in mouse xenografts. DLG1-AS1 functions as a competing endogenous RNA (ceRNA) for miR-497. Further investigation revealed that DLG1-AS1 regulated yes-associated protein 1 (YAP1; a known target of miR-497) by competitively binding to miR-497. Moreover, inhibition of miR-497 abrogated the inhibitory effects of DLG1-AS1 depletion on PTC cells. These findings demonstrate that the DLG1-AS1&#x2013;miR-497&#x2013;YAP1 axis promotes the growth and metastasis of PTC by forming a ceRNA network.
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Intratumoral levels and prognostic significance of Fusobacterium nucleatum in cervical carcinoma

Shu-Ting Huang, Jing Chen, Li-Yin Lian, Hui-Hua Cai, Hai-Shan Zeng, Min Zheng, Mu-Biao Liu,

https://doi.org/10.18632/aging.104188 pp 23337—23350

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Huang S, Chen J, Lian L, Cai H, Zeng H, Zheng M, Liu M, . Intratumoral levels and prognostic significance of Fusobacterium nucleatum in cervical carcinoma. . 12:23337-23350. https://doi.org/10.18632/aging.104188

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Provider: 
 TY - JOUR
 AU - Huang, Shu-Ting 
 AU - Chen, Jing 
 AU - Lian, Li-Yin 
 AU - Cai, Hui-Hua 
 AU - Zeng, Hai-Shan 
 AU - Zheng, Min 
 AU - Liu, Mu-Biao 
 TI - Intratumoral levels and prognostic significance of Fusobacterium nucleatum in cervical carcinoma
 JO - 
 JA - 
 VL - 12
 IS - 22
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104188
 DO - 10.18632/aging.104188
 SP - 23337
 EP - 23350
 PY - 
 AB - Growing evidence suggests that microbes can influence the onset of cancer and its consequent development. By researching samples from patients afflicted by cervical cancer, we aimed to explore the associated dynamics and prognostic value of intratumoral levels of F. nucleatum. We used qPCR to analyze tumor tissues obtained from 112 cervical cancer patients in order to characterize the levels and influences of intratumoral levels of the F. nucleatum. Especially for recurrent tissues, there was a distinct observation of higher levels of F. nucleatum in cervical cancer. Patients with high burdens of F. nucleatum intratumoral infiltration exhibited correspondingly poor rates of both overall survival and progression-free survival. Measures of the levels of F. nucleatum were found to have been reliable independent prognostic factors that could predict rates of PFS for afflicted patients (HR = 4.8, 95%CI = 1.2-18.6, P = 0.024). Notably, the levels of F. nucleatum were positively correlated with tumor differentiation. Cancer cells from patients with relatively high levels of F. nucleatum were observed to possess the characteristics of cancer stem cells (CSCs). We propose that F. nucleatum might be one potential cervical cancer diagnostic and prognostic biomarker, and these findings will help to provide a sound rationale and merit for further study of this bacterium.
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Cognitive reserve and network efficiency as compensatory mechanisms of the effect of aging on phonemic fluency

Lissett Gonzalez-Burgos, José Barroso, Daniel Ferreira,

https://doi.org/10.18632/aging.202177 pp 23351—23378

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Gonzalez-Burgos L, Barroso J, Ferreira D, . Cognitive reserve and network efficiency as compensatory mechanisms of the effect of aging on phonemic fluency. . 12:23351-23378. https://doi.org/10.18632/aging.202177

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                TY  - JOUR
                AU  - Gonzalez-Burgos, Lissett 
                AU  - Barroso, José 
                AU  - Ferreira, Daniel 
                TI  - Cognitive reserve and network efficiency as compensatory mechanisms of the effect of aging on phonemic fluency
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202177
                DO  - 10.18632/aging.202177
                SP  - 23351
                EP  - 23378
                PY  - 
                AB  - Compensation in cognitive aging is a topic of recent interest. However, factors contributing to cognitive compensation in functions such as phonemic fluency (PF) are not completely understood. Using cross-sectional data, we investigated cognitive reserve (CR) and network efficiency in young (32-58 years) versus old (59-84 years) individuals with high versus low performance in PF. ANCOVA was used to investigate the interaction between CR, age, and performance in PF. Random forest and graph theory analyses were conducted to study the contribution of cognition to PF and efficiency measures, respectively. Higher CR increased performance in PF and reduced age-related differences in PF. A slightly higher number of cognitive functions contributed to performance in high CR groups. The networks were more integrated in high CR individuals, both in the older age and high-performance groups. The strength and segregation of the networks were decreased in high-performance groups with high CR. We conclude that PF decreases less with age in individuals with higher CR, possibly due to a greater capacity to recruit non-linguistic cognitive networks, and efficient use of language networks, thereby integrating information in a rapid way across less fragmented networks. High CR and network efficiency seem to be important factors for cognitive compensation.
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Radiation-induced skin injury: pathogenesis, treatment, and management

Xiaojing Yang, Hanru Ren, Xiaomao Guo, Chaosu Hu, Jie Fu,

https://doi.org/10.18632/aging.103932 pp 23379—23393

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Yang X, Ren H, Guo X, Hu C, Fu J, . Radiation-induced skin injury: pathogenesis, treatment, and management. . 12:23379-23393. https://doi.org/10.18632/aging.103932

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                TY  - JOUR
                AU  - Yang, Xiaojing 
                AU  - Ren, Hanru 
                AU  - Guo, Xiaomao 
                AU  - Hu, Chaosu 
                AU  - Fu, Jie 
                TI  - Radiation-induced skin injury: pathogenesis, treatment, and management
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103932
                DO  - 10.18632/aging.103932
                SP  - 23379
                EP  - 23393
                PY  - 
                AB  - Radiation-induced skin injury (RSI) refers to a frequently occurring complication of radiation therapy. Nearly 90% of patients having received radiation therapy underwent moderate-to-severe skin reactions, severely reducing patients' quality of life and adversely affecting their disease treatment. No gold standard has been formulated for RSIs. In the present study, the mechanism of RSI and topical medications was discussed. Besides, this study can be referenced for clinicians to treat RSIs to guide subsequent clinical medicine.
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Circulating plasma factors involved in rejuvenation

Jae Sook Kang, Yong Ryoul Yang,

https://doi.org/10.18632/aging.103933 pp 23394—23408

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Kang JS, Yang YR, . Circulating plasma factors involved in rejuvenation. . 12:23394-23408. https://doi.org/10.18632/aging.103933

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                TY  - JOUR
                AU  - Kang, Jae Sook 
                AU  - Yang, Yong Ryoul 
                TI  - Circulating plasma factors involved in rejuvenation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103933
                DO  - 10.18632/aging.103933
                SP  - 23394
                EP  - 23408
                PY  - 
                AB  - Aging is defined as a time-dependent functional decline that occurs in many physiological systems. This decline is the primary risk factor for prominent human pathologies such as cancer, metabolic disorders, cardiovascular disorders, and neurodegenerative diseases. Aging and age-related diseases have multiple causes. Parabiosis experiments, in which the circulatory systems of young and old mice were surgically joined, revealed that young plasma counteracts aging and rejuvenates organs in old mice, suggesting the existence of rejuvenating factors that become less abundant with aging. Diverse approaches have identified a large number of plasma proteins whose levels differ significantly between young and old mice, as well as numerous rejuvenating factors that reverse aged-related impairments in multiple tissues. These observations suggest that increasing the levels of key rejuvenating factors could promote restorative biological processes or inhibit pathological degeneration. Inspired by such findings, several companies have begun selling &#x201C;young blood transfusions,&#x201D; and others have tested young plasma as a treatment for Alzheimer&#x2019;s disease. Here, we summarize the current findings regarding rejuvenating factors.
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COVID-19
Impact of cardiovascular and metabolic diseases on the severity of COVID-19: a systematic review and meta-analysis

Meng Meng, Qianwen Zhao, Rahul Kumar, Chen Bai, Yunlei Deng, Bo Wan,

https://doi.org/10.18632/aging.103991 pp 23409—23421

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Meng M, Zhao Q, Kumar R, Bai C, Deng Y, Wan B, . Impact of cardiovascular and metabolic diseases on the severity of COVID-19: a systematic review and meta-analysis. . 12:23409-23421. https://doi.org/10.18632/aging.103991

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                TY  - JOUR
                AU  - Meng, Meng 
                AU  - Zhao, Qianwen 
                AU  - Kumar, Rahul 
                AU  - Bai, Chen 
                AU  - Deng, Yunlei 
                AU  - Wan, Bo 
                TI  - Impact of cardiovascular and metabolic diseases on the severity of COVID-19: a systematic review and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103991
                DO  - 10.18632/aging.103991
                SP  - 23409
                EP  - 23421
                PY  - 
                AB  - We examined the effects of coronary heart disease (CHD), hypertension and diabetes on the development of severe COVID-19. We performed a comprehensive, systematic literature search for studies published between December 2019 and July 5, 2020 in five databases. The prevalence of severe COVID-19 in patients with CHD, hypertension and diabetes was evaluated through a meta-analysis. Thirty-five articles with 8,170 patients were included, and all the available studies were case series. The pooled odds ratio for the development of severe COVID-19 was 3.21 for patients with CHD (fixed-effects model, 95% CI: 2.58-3.99), 2.27 for patients with hypertension (random-effects model, 95% CI: 1.79-2.90) and 2.34 for patients with diabetes (random-effects model, 95% CI: 1.79-3.05). The heterogeneity of the studies was moderate for the effect of CHD on COVID-19 severity, but was high for the effects of diabetes and hypertension. Funnel plots and Egger&#x2019;s tests revealed no publication bias in the CHD and hypertension analyses, but suggested publication bias in the diabetes analysis. This bias was corrected using the trim-and-fill method, and was ultimately found to have no effect on the results. Our findings suggest patients with CHD, hypertension and diabetes are at greater risk for developing severe COVID-19 than those without these conditions.
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Volume 12, Issue 22

About the Cover

Editorials

Nico P. Dantuma, Thorsten Hoppe, Laura K. Herzog,

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Oliver Robinson, Chung-Ho E. Lau,

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Niels van den Berg,

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Theory Article

Richard S. Criddle, Hsien-Jung L. Lin, Isabella James, Ji Sun Park, Lee D. Hansen, John C. Price,

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Research Papers

COVID-19 Genomic, epigenomic, and immune subtype analysis of CTSL/B and SARS-CoV-2 receptor ACE2 in pan-cancer

Huimin Li, Longxiang Xie, Lin Chen, Lu Zhang, Yali Han, Zhongyi Yan, Xiangqian Guo,

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COVID-19 High incidence of stroke in COVID-19 patients

Jingyu Chen, Yazhou Wu, Zhi Chen, Bin Yi, Lili Zhang, Changlin Yin, Hua Feng,

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COVID-19 Impact of age on duration of viral RNA shedding in patients with COVID-19

Chenliang Zhou, Tianfang Zhang, Haotang Ren, Shanshan Sun, Xia Yu, Jifang Sheng, Yu Shi, Hong Zhao,

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COVID-19 Clinical characteristics of the first known cases of death caused by COVID-19 pneumonia

Fan-Zhen Kong, Yi Wang, Mei-Xia Wang, Qing-Zhang Cheng, Robert Logan, Guan-Hui Wu, Si-Ming Hu,

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COVID-19 Estimating the release of inflammatory factors and use of glucocorticoid therapy for COVID-19 patients with comorbidities

Dan Han, Chunfen Peng, Rui Meng, Jing Yao, Qiong Zhou, Yong Xiao, Hong Ma,

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COVID-19 In search of preventive strategies: novel high-CBD Cannabis sativa extracts modulate ACE2 expression in COVID-19 gateway tissues

Bo Wang, Anna Kovalchuk, Dongping Li, Rocio Rodriguez-Juarez, Yaroslav Ilnytskyy, Igor Kovalchuk, Olga Kovalchuk,

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Yafit Hachmo, Amir Hadanny, Ramzia Abu Hamed, Malka Daniel-Kotovsky, Merav Catalogna, Gregory Fishlev, Erez Lang, Nir Polak, Keren Doenyas, Mony Friedman, Yonatan Zemel, Yair Bechor, Shai Efrati,

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Afsaneh Mohammadnejad, Marianne Nygaard, Shuxia Li, Dongfeng Zhang, Chunsheng Xu, Weilong Li, Jesper Lund, Lene Christiansen, Jan Baumbach, Kaare Christensen, Jacob v. B. Hjelmborg, Qihua Tan,

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Eva Bártová, Soňa Legartová, Jana Krejčí, Orazio Angelo Arcidiacono,

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Jian Zhang, Xi Zhong, Huali Jiang, Hualong Jiang, Tao Xie, Yunhong Tian, Rong Li, Baiyao Wang, Jiexia Zhang, Yawei Yuan,

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Yuejiang Zhao, Hanwen Chen, Lu Wang, Zhiyuan Guo, Shijie Liu, Simin Luo,

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Lushuang Xie, Ning Zhang, Qun Zhang, Chenyu Li, Aaron F. Sandhu, George Williams III, Sirui Lin, PeiRan Lv, Yi Liu, Qiaofeng Wu, Shuguang Yu,

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Shan Zhong, Jun Xue, Jiao-Jiao Cao, Bomin Sun, Qing-Fang Sun, Liu-Guan Bian, Liang-Yun Hu, Si-Jian Pan,

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Zhiping Zhao, Junfeng Zhang, Liangyu Yin, Jiali Yang, Yao Zheng, Mengjie Zhang, Bing Ni, Huaizhi Wang,

COVID-19
Genomic, epigenomic, and immune subtype analysis of CTSL/B and SARS-CoV-2 receptor ACE2 in pan-cancer

COVID-19
High incidence of stroke in COVID-19 patients

COVID-19
Impact of age on duration of viral RNA shedding in patients with COVID-19

COVID-19
Clinical characteristics of the first known cases of death caused by COVID-19 pneumonia

COVID-19
Estimating the release of inflammatory factors and use of glucocorticoid therapy for COVID-19 patients with comorbidities

COVID-19
In search of preventive strategies: novel high-CBD Cannabis sativa extracts modulate ACE2 expression in COVID-19 gateway tissues