Volume 11, Issue 19

Provider: 
                TY  - JOUR
                AU  - Blagosklonny, Mikhail V. 
                TI  - Rapamycin for longevity: opinion article
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102355
                DO  - 10.18632/aging.102355
                SP  - 8048
                EP  - 8067
                PY  - 
                AB  - From the dawn of civilization, humanity has dreamed of immortality. So why didn&#x2019;t the discovery of the anti-aging properties of mTOR inhibitors change the world forever? I will discuss several reasons, including fear of the actual and fictional side effects of rapamycin, everolimus and other clinically-approved drugs, arguing that no real side effects preclude their use as anti-aging drugs today. Furthermore, the alternative to the reversible (and avoidable) side effects of rapamycin/everolimus are the irreversible (and inevitable) effects of aging: cancer, stroke, infarction, blindness and premature death. I will also discuss why it is more dangerous not to use anti-aging drugs than to use them and how rapamycin-based drug combinations have already been implemented for potential life extension in humans. If you read this article from the very beginning to its end, you may realize that the time is now.
                ER  -

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

A circular RNA from APC inhibits the proliferation of diffuse large B-cell lymphoma by inactivating Wnt/β-catenin signaling via interacting with TET1 and miR-888

Yanping Hu, Yixun Zhao, Chao Shi, Pengfei Ren, Bing Wei, Yongjun Guo, Jie Ma,

https://doi.org/10.18632/aging.102122 pp 8068—8084

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Hu Y, Zhao Y, Shi C, Ren P, Wei B, Guo Y, Ma J, . A circular RNA from APC inhibits the proliferation of diffuse large B-cell lymphoma by inactivating Wnt/β-catenin signaling via interacting with TET1 and miR-888. . 11:8068-8084. https://doi.org/10.18632/aging.102122

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Hu, Yanping 
 AU - Zhao, Yixun 
 AU - Shi, Chao 
 AU - Ren, Pengfei 
 AU - Wei, Bing 
 AU - Guo, Yongjun 
 AU - Ma, Jie 
 TI - A circular RNA from APC inhibits the proliferation of diffuse large B-cell lymphoma by inactivating Wnt/β-catenin signaling via interacting with TET1 and miR-888
 JO - 
 JA - 
 VL - 11
 IS - 19
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102122
 DO - 10.18632/aging.102122
 SP - 8068
 EP - 8084
 PY - 
 AB - Circular RNA (circRNA), a type of non-coding RNA, can promote or suppress tumorigenesis. To investigate the involvement of circRNA in diffuse large B-cell lymphoma (DLBCL), we performed a circRNA microarray analysis on paired DLBCL and normal tissues. We identified a novel and highly stable circRNA originating from the back-splicing of APC exon 7 to exon 14, circ-APC (hsa_circ_0127621), which was downregulated in DLBCL tissues, cell lines and plasma. In gain-of-function experiments, ectopic expression of circ-APC inhibited DLBCL cell proliferation in vitro and tumor growth in vivo. Cytoplasmic circ-APC functioned as a sponge for miR-888, thus post-transcriptionally upregulating APC by alleviating the repressive effects of miR-888 on this gene. Further, nuclear circ-APC bound to the APC promoter and recruited the DNA demethylase TET1, thereby transcriptionally upregulating APC. Upon its upregulation, APC dampened the canonical Wnt/&#x3B2;-catenin signaling pathway by reducing the accumulation of &#x3B2;-catenin in the nucleus, thereby retarding DLBCL growth. Clinically, circ-APC was found to be an effective diagnostic and prognostic biomarker for patients with DLBCL. Our study suggests that circ-APC is a novel proliferation inhibitor, and that restoring circ-APC expression may be a promising therapeutic approach for DLBCL patients.
 ER -

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

Oxidative stress-induced cellular senescence desensitizes cell growth and migration of vascular smooth muscle cells through down-regulation of platelet-derived growth factor receptor-beta

Chun-Hsu Pan, Chang-Jui Chen, Chun-Ming Shih, Ming-Fu Wang, Jie-Yu Wang, Chieh-Hsi Wu,

https://doi.org/10.18632/aging.102270 pp 8085—8102

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Pan C, Chen C, Shih C, Wang M, Wang J, Wu C, . Oxidative stress-induced cellular senescence desensitizes cell growth and migration of vascular smooth muscle cells through down-regulation of platelet-derived growth factor receptor-beta. . 11:8085-8102. https://doi.org/10.18632/aging.102270

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Pan, Chun-Hsu 
                AU  - Chen, Chang-Jui 
                AU  - Shih, Chun-Ming 
                AU  - Wang, Ming-Fu 
                AU  - Wang, Jie-Yu 
                AU  - Wu, Chieh-Hsi 
                TI  - Oxidative stress-induced cellular senescence desensitizes cell growth and migration of vascular smooth muscle cells through down-regulation of platelet-derived growth factor receptor-beta
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102270
                DO  - 10.18632/aging.102270
                SP  - 8085
                EP  - 8102
                PY  - 
                AB  - The relationship between aging and restenosis are unclear. The purposes of this study were to investigate the possible pathological role and mechanism of aging on formation of restenosis. Our data indicated that cell proliferation and migration of the oxidative stress-induced senescent vascular smooth muscle cells were obviously desensitized to stimulation by platelet-derived growth factor (PDGF)-BB, which may have been caused by suppression of promoter activity, transcription, translation, and activation levels of PDGF receptor (PDGFR)-&#x3B2;. The analyzed data obtained from the binding array of transcription factors (TFs) showed that binding levels of eighteen TFs on the PDGFR-&#x3B2; promoter region (-523 to -1) were significantly lower in senescent cells compared to those of non-senescent cells. Among these TFs, the bioinformatics prediction suggested that the putative binding sites of ten TFs were found in this promoter region. Of these, transcriptional levels of seven TFs were markedly reduced in senescent cells. The clinical data showed that the proportion of restenosis was relatively lower in the older group than that in the younger group. Our study results suggested that a PDGFR-&#x3B2;-mediated pathway was suppressed in aging cells, and our clinical data showed that age and the vascular status were slightly negatively correlated in overall participants.
                ER  -

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

Disulfiram suppressed ethanol promoted RANKL-induced osteoclastogenesis in vitro and ethanol-induced osteoporosis in vivo via ALDH1A1-NFATc1 axis

Yewei Jia, Jiawei Jiang, Kangxian Zhao, Tan Zhang, Peng Sun, Jiaxuan Peng, Qichang Yang, Yu Qian,

https://doi.org/10.18632/aging.102279 pp 8103—8119

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Jia Y, Jiang J, Zhao K, Zhang T, Sun P, Peng J, Yang Q, Qian Y, . Disulfiram suppressed ethanol promoted RANKL-induced osteoclastogenesis in vitro and ethanol-induced osteoporosis in vivo via ALDH1A1-NFATc1 axis. . 11:8103-8119. https://doi.org/10.18632/aging.102279

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Jia, Yewei 
                AU  - Jiang, Jiawei 
                AU  - Zhao, Kangxian 
                AU  - Zhang, Tan 
                AU  - Sun, Peng 
                AU  - Peng, Jiaxuan 
                AU  - Yang, Qichang 
                AU  - Qian, Yu 
                TI  - Disulfiram suppressed ethanol promoted RANKL-induced osteoclastogenesis in vitro and ethanol-induced osteoporosis in vivo via ALDH1A1-NFATc1 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102279
                DO  - 10.18632/aging.102279
                SP  - 8103
                EP  - 8119
                PY  - 
                AB  - Excessive alcohol consumption is positively related to osteoporosis, and its treatment strategies are poorly developed. Disulfiram inhibits receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis; however, whether it can be used for ethanol-induced osteoclastogenesis and its underlying mechanism are still unclear. In this study, we demonstrated that ethanol promoted RANKL-induced osteoclast formation and bone resorption, whereas, disulfiram suppressed ethanol-induced osteoclastogenesis by abrogating the expression of nuclear factor of activated T cell c1 (NFATc1) in vitro. Further analysis revealed that aldehyde dehydrogenase 1A1 (ALDH1A1) is important for the expression of NFATc1, the master regulator of osteoclast differentiation. Furthermore, we showed that disulfiram protected ethanol-induced osteoporosis in vivo. Overall, our study provides promising evidence that disulfiram can be used as a treatment strategy for alcohol-related osteoporosis via the ALDH1A1T&#x2013;NFATc1 axis.
                ER  -

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

The interaction between STAT3 and nAChRα1 interferes with nicotine-induced atherosclerosis via Akt/mTOR signaling cascade

Shuang Xu, Huaner Ni, Hangwei Chen, Qiuyan Dai,

https://doi.org/10.18632/aging.102296 pp 8120—8138

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu S, Ni H, Chen H, Dai Q, . The interaction between STAT3 and nAChRα1 interferes with nicotine-induced atherosclerosis via Akt/mTOR signaling cascade. . 11:8120-8138. https://doi.org/10.18632/aging.102296

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xu, Shuang 
                AU  - Ni, Huaner 
                AU  - Chen, Hangwei 
                AU  - Dai, Qiuyan 
                TI  - The interaction between STAT3 and nAChRα1 interferes with nicotine-induced atherosclerosis via Akt/mTOR signaling cascade
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102296
                DO  - 10.18632/aging.102296
                SP  - 8120
                EP  - 8138
                PY  - 
                AB  - During atherosclerosis development, nicotine and its &#x3B1;1 nicotinic acetylcholine receptors (nAChR&#x3B1;1) activate atherogenic inflammation. However, the effect of signal transducer and activator of transcription 3 (STAT3)-related inflammatory pathways in nicotine-induced atherosclerosis has been poorly studied. This study investigated the transcriptional mechanism of STAT3 in nicotine/nAChR&#x3B1;1-induced atherosclerosis. In vivo, ApoE-/- mice were used to establish an atherosclerotic model. Plaque area and composition were assessed by oil red O staining and immunohistochemistry. In vitro, vascular smooth muscle cells and macrophages were used to investigate cell migration, proliferation, inflammation and related signaling pathways by Transwell migration assay, EdU assay, immunofluorescence, western blotting, coimmunoprecipitation and chromatin immunoprecipitation. nAChR&#x3B1;1 knockdown significantly decreases the nicotine-induced upregulation of p-STAT3, p-Akt and p-mTOR in vitro, while nAChR&#x3B1;1 overexpression has the opposite effects. The inhibition of STAT3 attenuated nicotine-induced atherosclerosis, by reducing the proliferation and migration of vascular smooth muscle cells and inflammation in macrophages. Moreover, there is a direct interaction between STAT3 and nAChR&#x3B1;1 that modulates STAT3 nuclear translocation and its binding to the Akt promoter region upon nicotine exposure. Taken together, STAT3 and nAChR&#x3B1;1 blockade attenuates nicotine-induced atherosclerosis by reducing the migration and proliferation of vascular smooth muscle cells and inflammation in macrophages via the Akt/mTOR pathway.
                ER  -

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

Hypermethylated long noncoding RNA MEG3 promotes the progression of gastric cancer

Lei Ding, Yuan Tian, Ling Wang, Miaomiao Bi, Dengke Teng, Sen Hong,

https://doi.org/10.18632/aging.102309 pp 8139—8155

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ding L, Tian Y, Wang L, Bi M, Teng D, Hong S, . Hypermethylated long noncoding RNA MEG3 promotes the progression of gastric cancer. . 11:8139-8155. https://doi.org/10.18632/aging.102309

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ding, Lei 
                AU  - Tian, Yuan 
                AU  - Wang, Ling 
                AU  - Bi, Miaomiao 
                AU  - Teng, Dengke 
                AU  - Hong, Sen 
                TI  - Hypermethylated long noncoding RNA MEG3 promotes the progression of gastric cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102309
                DO  - 10.18632/aging.102309
                SP  - 8139
                EP  - 8155
                PY  - 
                AB  - This study aims to explore the expression and degree of methylation of lncRNA MEG3 in gastric cancer tissues and to analyze its effect on the migration and proliferation of gastric cancer patients and the mechanism by which this occurs. The targeting relationship between MEG3, miR-181a-5p and ATP4B was detected through molecular biology experiments. Wound healing, transwell, colony formation and flow cytometry assays were used to analyze the effects of lncRNA MEG3 and methylation on tumor cell migration, invasion, proliferation and apoptosis. In addition, a tumor xenotransplantation model was established to study the influence of MEG3 on tumor growth in vivo. Bioinformatics analysis showed that lncRNA MEG3 and ATP4B were downregulated in gastric cancer tissues compared with normal tissues. Bioinformatics predicted that ATP4B might be regulated by targeting miR-181a-5p. The overexpression of MEG3 and the application of 5-Aza treatment inhibited the migration, invasion and proliferation of MGC-803 cells and promoted apoptosis. In gastric cancer tissues, MEG3 is hypermethylated to decrease expression. Once the expression of MEG3 is restored or methylation is inhibited, tumor growth can be inhibited both in vivo and in vitro. This finding could be utilized as a clinical reference for gastric cancer treatment in the future.
                ER  -

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

Knockdown of CREB3 activates endoplasmic reticulum stress and induces apoptosis in glioblastoma

Yaxin Hu, Liangzhao Chu, Jian Liu, Lei Yu, Shi-bin Song, Hua Yang, Feng Han,

https://doi.org/10.18632/aging.102310 pp 8156—8168

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Hu Y, Chu L, Liu J, Yu L, Song S, Yang H, Han F, . Knockdown of CREB3 activates endoplasmic reticulum stress and induces apoptosis in glioblastoma. . 11:8156-8168. https://doi.org/10.18632/aging.102310

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Hu, Yaxin 
 AU - Chu, Liangzhao 
 AU - Liu, Jian 
 AU - Yu, Lei 
 AU - Song, Shi-bin 
 AU - Yang, Hua 
 AU - Han, Feng 
 TI - Knockdown of CREB3 activates endoplasmic reticulum stress and induces apoptosis in glioblastoma
 JO - 
 JA - 
 VL - 11
 IS - 19
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102310
 DO - 10.18632/aging.102310
 SP - 8156
 EP - 8168
 PY - 
 AB - Glioblastoma is a highly malignant type of central nervous system tumor. In the present study, the results of RNA sequencing indicated that cAMP responsive element binding protein 3 (CREB3) was upregulated in tumor tissues from patients with GBM. The cAMP responsive element binding protein 3 (CREB3) pathway is a major contributor to the malignant progression of glioblastoma. In this study, we explored the mechanisms by which CREB3 regulates the proliferation, invasion and apoptosis of glioblastoma. Pairs of glioblastoma and normal tissues were subjected to RNA sequencing. Then, qRT-PCR and Western blotting were used to detect CREB3 levels in glioblastoma tissues and cell lines, respectively. CREB3 was upregulated in glioblastoma tissues and cell lines. Overexpression of CREB3 promoted the proliferation and invasion of SHG-44 cells, while downregulation of CREB3 inhibited the invasion of U251MG cells. Knockdown of CREB3 also induced apoptosis in U251MG cells and increased the protein levels of BAX, active caspase 3, p-PERK, p-eIF2&#x3B1; and ATF4. An in vivo study in nude mice bearing U251MG cell xenografts confirmed these results. Our findings indicate that CREB3 functions as a tumor promoter in glioblastoma, and thus could serve as a treatment target in glioblastoma patients.
 ER -

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

KCNK levels are prognostic and diagnostic markers for hepatocellular carcinoma

Wen-Chao Li, Zhi-Yong Xiong, Pin-Zhu Huang, Yang-Jing Liao, Quan-Xi Li, Zhi-Cheng Yao, Ya-Di Liao, Shi-Lei Xu, Hui Zhou, Qing-Liang Wang, He Huang, Peng Zhang, Ji-Zong Lin, Bo Liu, Jie Ren, Kun-Peng Hu,

https://doi.org/10.18632/aging.102311 pp 8169—8182

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li W, Xiong Z, Huang P, Liao Y, Li Q, Yao Z, Liao Y, Xu S, Zhou H, Wang Q, Huang H, Zhang P, Lin J, et al, . KCNK levels are prognostic and diagnostic markers for hepatocellular carcinoma. . 11:8169-8182. https://doi.org/10.18632/aging.102311

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Wen-Chao 
                AU  - Xiong, Zhi-Yong 
                AU  - Huang, Pin-Zhu 
                AU  - Liao, Yang-Jing 
                AU  - Li, Quan-Xi 
                AU  - Yao, Zhi-Cheng 
                AU  - Liao, Ya-Di 
                AU  - Xu, Shi-Lei 
                AU  - Zhou, Hui 
                AU  - Wang, Qing-Liang 
                AU  - Huang, He 
                AU  - Zhang, Peng 
                AU  - Lin, Ji-Zong 
                AU  - Liu, Bo 
                AU  - Ren, Jie 
                AU  - Hu, Kun-Peng 
                TI  - KCNK levels are prognostic and diagnostic markers for hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102311
                DO  - 10.18632/aging.102311
                SP  - 8169
                EP  - 8182
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Wen-Chao 
                AU  - Xiong, Zhi-Yong 
                AU  - Huang, Pin-Zhu 
                AU  - Liao, Yang-Jing 
                AU  - Li, Quan-Xi 
                AU  - Yao, Zhi-Cheng 
                AU  - Liao, Ya-Di 
                AU  - Xu, Shi-Lei 
                AU  - Zhou, Hui 
                AU  - Wang, Qing-Liang 
                AU  - Huang, He 
                AU  - Zhang, Peng 
                AU  - Lin, Ji-Zong 
                AU  - Liu, Bo 
                AU  - Ren, Jie 
                AU  - Hu, Kun-Peng 
                TI  - KCNK levels are prognostic and diagnostic markers for hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102311
                DO  - 10.18632/aging.102311
                SP  - 8169
                EP  - 8182
                PY  - 
                AB  - Two-pore-domain (KCNK, K2P) K+ channels are transmembrane protein complexes that control the flow of ions across biofilms, which underlie many essential cellular functions. Because KCNK family members are known to contribute to tumorigenesis in various types of cancer, we hypothesized that they might be differentially expressed in hepatocellular carcinoma (HCC) cells as compared to healthy tissue and serve as diagnostic or prognostic biomarkers. We tested this hypothesis through bioinformatic analyses of publicly available data for the expression of various KCNK subunits in HCC. We observed reduced expression of KCNK2, KCNK15, and KCNK17 in liver cancer, as well as overexpression of KCNK9, all of which correlated with a better prognosis for HCC patients per survival analyses. Moreover, ROC curves indicated that KCNK2, KCNK9, KCNK15, and KCNK17 levels could be used as a diagnostic biomarker for HCC. Finally, our western blot and qRT-PCR results were consistent with those obtained from bioinformatic analyses. Taken together, these results suggest that KCNK2, KCNK9, KCNK15, and KCNK17 could serve as potential diagnostic and prognostic biomarkers of HCC.
                ER  -

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

CircRNA Cdr1as functions as a competitive endogenous RNA to promote hepatocellular carcinoma progression

Yang Su, Xiurui Lv, Wei Yin, Lingling Zhou, Yilin Hu, Ang Zhou, FuZhen Qi,

https://doi.org/10.18632/aging.102312 pp 8183—8203

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Su Y, Lv X, Yin W, Zhou L, Hu Y, Zhou A, Qi F, . CircRNA Cdr1as functions as a competitive endogenous RNA to promote hepatocellular carcinoma progression. . 11:8183-8203. https://doi.org/10.18632/aging.102312

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Su, Yang 
                AU  - Lv, Xiurui 
                AU  - Yin, Wei 
                AU  - Zhou, Lingling 
                AU  - Hu, Yilin 
                AU  - Zhou, Ang 
                AU  - Qi, FuZhen 
                TI  - CircRNA Cdr1as functions as a competitive endogenous RNA to promote hepatocellular carcinoma progression
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102312
                DO  - 10.18632/aging.102312
                SP  - 8183
                EP  - 8203
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Recent years, circular RNA (circRNA) have been shown to exert vital functions in the pathological progressions of many diseases. A growing number of evidences have identified the representative function of exosomal circRNAs in the physiological state of donor cells, which further induces cellular responses after captured by recipient cells. However, the contributions of circRNAs to HCC remain largely unknown. In vitro and in vivo regulatory roles of circRNA Cdr1as in proliferative and migratory abilities of HCC were evaluated by CCK8, EdU, Transwell and tumourigenicity assays, respectively. Results showed circRNA Cdr1as was highly expressed in HCC cell lines and tissues. Overexpression of circRNA Cdr1as greatly accelerated HCC cells to proliferate and migrate. Mechanistically, we found that Cdr1as could promote the expression of AFP, a well-known biomarker for HCC, by sponging miR-1270. Further studies showed exosomes extracted from HCC cells overexpressing circRNA Cdr1as accelerated the proliferative and migratory abilities of surrounding normal cells. In all, circRNA Cdr1as serves as a ceRNA to promote the progression of HCC. Meanwhile, it is directly transferred from HCC cells to surrounding normal cells via exosomes to further mediate the biological functions of surrounding cells.
                ER  -

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

SNHG22 overexpression indicates poor prognosis and induces chemotherapy resistance via the miR-2467/Gal-1 signaling pathway in epithelial ovarian carcinoma

Peng-Fei Zhang, Jing Wu, Jin-Hong Luo, Ke-Sang Li, Fei Wang, Wei Huang, Yin Wu, Shui-Ping Gao, Xue-Mei Zhang, Peng-Nan Zhang,

https://doi.org/10.18632/aging.102313 pp 8204—8216

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhang P, Wu J, Luo J, Li K, Wang F, Huang W, Wu Y, Gao S, Zhang X, Zhang P, . SNHG22 overexpression indicates poor prognosis and induces chemotherapy resistance via the miR-2467/Gal-1 signaling pathway in epithelial ovarian carcinoma. . 11:8204-8216. https://doi.org/10.18632/aging.102313

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhang, Peng-Fei 
                AU  - Wu, Jing 
                AU  - Luo, Jin-Hong 
                AU  - Li, Ke-Sang 
                AU  - Wang, Fei 
                AU  - Huang, Wei 
                AU  - Wu, Yin 
                AU  - Gao, Shui-Ping 
                AU  - Zhang, Xue-Mei 
                AU  - Zhang, Peng-Nan 
                TI  - SNHG22 overexpression indicates poor prognosis and induces chemotherapy resistance via the miR-2467/Gal-1 signaling pathway in epithelial ovarian carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102313
                DO  - 10.18632/aging.102313
                SP  - 8204
                EP  - 8216
                PY  - 
                AB  - Recently, an increasing number of studies have reported that dysregulation of long noncoding RNAs (lncRNAs) plays an important role in cancer initiation and progression, including in epithelial ovarian carcinoma (EOC). However, little is known about the detailed biological functions of the lncRNA small nucleolar RNA host gene 22 (SNHG22) during the progression of EOC. Here, we found that SNHG22 was significantly increased in EOC tissues and was significantly associated with a low level of differentiation. Forced SNHG22 expression promoted chemotherapy resistance in EOC cells. Knockdown of SNHG22 expression increased the sensitivity of EOC cells to cisplatin and paclitaxel. Importantly, we found that SNHG22 could directly interact with miR-2467 and lead to the release of miR-2467-targeted Gal-1 mRNA. Moreover, SNHG22 overexpression induced EOC cell resistance to chemotherapy agents via PI3K/AKT and ERK cascade activation. In summary, our findings demonstrate that SNHG22 plays a critical role in the chemotherapy resistance of EOC by mediating the miR-2467/Gal-1 regulatory axis.
                ER  -

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

Association between bone mineral density and brain parenchymal atrophy and ventricular enlargement in healthy individuals

In-Suk Bae, Jae Min Kim, Jin Hwan Cheong, Je Il Ryu, Myung-Hoon Han,

https://doi.org/10.18632/aging.102316 pp 8217—8238

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Bae I, Kim JM, Cheong JH, Ryu JI, Han M, . Association between bone mineral density and brain parenchymal atrophy and ventricular enlargement in healthy individuals. . 11:8217-8238. https://doi.org/10.18632/aging.102316

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Bae, In-Suk 
                AU  - Kim, Jae Min 
                AU  - Cheong, Jin Hwan 
                AU  - Ryu, Je Il 
                AU  - Han, Myung-Hoon 
                TI  - Association between bone mineral density and brain parenchymal atrophy and ventricular enlargement in healthy individuals
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102316
                DO  - 10.18632/aging.102316
                SP  - 8217
                EP  - 8238
                PY  - 
                AB  - Bone, vascular smooth muscle, and arachnoid trabeculae are composed of the same type of collagen. However, no studies have investigated the relationship between bone mineral density deterioration and cerebral atrophy, both of which occur in normal, healthy aging. Accordingly, we evaluated whether bone mineral density was associated with brain parenchymal atrophy and ventricular enlargement in healthy individuals. Intracranial cavity, brain parenchyma, and lateral ventricles volumes were measured using brain magnetic resonance imaging (MRI) with a semiautomated tool. We included 267 individuals with no history of dementia or other neurological diseases, who underwent one or more dual-energy X-ray absorptiometry scans and brain MRIs simultaneously (within 3 years of each other) at our hospital over an 11-year period. We found that progression of brain parenchymal atrophy was positively associated with bone mineral density after full adjustment (B, 0.94; P &lt; 0.001). In addition, individuals with osteoporosis showed more parenchymal atrophy among those younger than 80 years. In addition, we observed greater ventricular enlargement in individuals with osteoporosis among those older than 80 years. We believe that osteoporosis may play a role in the acceleration of parenchymal atrophy during the early-stages, and ventricular enlargement in the late-stages, of normal aging-related cerebral atrophy.
                ER  -

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

The long non-coding RNA, urothelial carcinoma associated 1, promotes cell growth, invasion, migration, and chemo-resistance in glioma through Wnt/β-catenin signaling pathway

Beilin Zhang, Shaokuan Fang, Yingying Cheng, Chunkui Zhou, Fang Deng,

https://doi.org/10.18632/aging.102317 pp 8239—8253

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhang B, Fang S, Cheng Y, Zhou C, Deng F, . The long non-coding RNA, urothelial carcinoma associated 1, promotes cell growth, invasion, migration, and chemo-resistance in glioma through Wnt/β-catenin signaling pathway. . 11:8239-8253. https://doi.org/10.18632/aging.102317

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhang, Beilin 
                AU  - Fang, Shaokuan 
                AU  - Cheng, Yingying 
                AU  - Zhou, Chunkui 
                AU  - Deng, Fang 
                TI  - The long non-coding RNA, urothelial carcinoma associated 1, promotes cell growth, invasion, migration, and chemo-resistance in glioma through Wnt/β-catenin signaling pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102317
                DO  - 10.18632/aging.102317
                SP  - 8239
                EP  - 8253
                PY  - 
                AB  - The long non-coding RNA, urothelial carcinoma associated 1 (UCA1) has been demonstrated to play important roles in various types of cancers. This study investigated the functional role of UCA1 in glioma and explored the underlying molecular mechanisms. UCA1 was found to be highly up-regulated in glioma cells, and knock-down of UCA1 inhibited cell growth, invasion and migration, and also induced apoptosis in glioma cells. On the other hand, overexpression of UCA1 promoted cell proliferation, cell invasion and migration in glioma cells. Knock-down of UCA1 suppressed the activity of Wnt/&#x3B2;-catenin signaling, and treatment with lithium chloride restored the inhibitory effect of UCA1 knock-down on cell invasion and migration. More importantly, the aberrant expression of UCA1 was associated with chemo-resistance to cisplatin and temozolomide in glioma cells via interacting with Wnt/&#x3B2;-catenin signaling. In vivo studies showed that overexpression of UCA1 promoted the in vivo tumor growth of U87 cells in the nude mice. Clinically, UCA1 was found to be up-regulated in glioma tissues and higher expression level of UCA1 was correlated with poor survival in patients with glioma. Taken together, our results showed that UCA1 had a functional role in the regulation of glioma cell growth, invasion and migration, and chemo-resistance possibly via Wnt/&#x3B2;-catenin signaling pathway.
                ER  -

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

Soluble klotho regulates the function of salivary glands by activating KLF4 pathways

Nguyen Chi Tai, Soo-A Kim, Sang-Gun Ahn,

https://doi.org/10.18632/aging.102318 pp 8254—8269

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Tai NC, Kim S, Ahn S, . Soluble klotho regulates the function of salivary glands by activating KLF4 pathways. . 11:8254-8269. https://doi.org/10.18632/aging.102318

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Tai, Nguyen Chi 
                AU  - Kim, Soo-A 
                AU  - Ahn, Sang-Gun 
                TI  - Soluble klotho regulates the function of salivary glands by activating KLF4 pathways
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102318
                DO  - 10.18632/aging.102318
                SP  - 8254
                EP  - 8269
                PY  - 
                AB  - The dysfunction of salivary glands commonly induces dry mouth, infections, and dental caries caused by a lack of saliva. This study was performed to determine the genetic and functional changes in salivary glands using a klotho (-/-) mouse model. Here, we confirmed the attenuation of KLF4 expression in the salivary glands of klotho (-/-) mice. Soluble klotho overexpression induced KLF4 transcription and KLF4-mediated signaling pathways, including mTOR, AMPK, and SOD1/2. Silencing klotho via siRNA significantly down-regulated KLF4 expression. Additionally, we monitored the function of salivary glands and soluble klotho and/or KLF4 responses and demonstrated that soluble klotho increased the expression of KLF4 and markers of salivary gland function (&#x3B1;-amylase, ZO-1, and Aqua5) in primary cultured salivary gland cells from wild type and klotho (-/-) mice. In a 3D culture system, cell sphere aggregates were observed in soluble klotho- or KLF4-expressing cells and exhibited higher expression levels of salivary gland function-related proteins than those in nontransfected cells. These results suggest that activation of the klotho-mediated KLF4 signaling pathway contributes to potentiating the function of salivary glands.
                ER  -

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

Systematic profiling of alternative splicing events and splicing factors in left- and right-sided colon cancer

Xiaoliang Huang, Jungang Liu, Xianwei Mo, Haizhou Liu, Chunyin Wei, Lingxu Huang, Jianhong Chen, Chao Tian, Yongsheng Meng, Guo Wu, Weishun Xie, Franco Jeen P.C., Zujun Liu, Weizhong Tang,

https://doi.org/10.18632/aging.102319 pp 8270—8293

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Huang X, Liu J, Mo X, Liu H, Wei C, Huang L, Chen J, Tian C, Meng Y, Wu G, Xie W, P.C. FJ, Liu Z, et al, . Systematic profiling of alternative splicing events and splicing factors in left- and right-sided colon cancer. . 11:8270-8293. https://doi.org/10.18632/aging.102319

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Huang, Xiaoliang 
                AU  - Liu, Jungang 
                AU  - Mo, Xianwei 
                AU  - Liu, Haizhou 
                AU  - Wei, Chunyin 
                AU  - Huang, Lingxu 
                AU  - Chen, Jianhong 
                AU  - Tian, Chao 
                AU  - Meng, Yongsheng 
                AU  - Wu, Guo 
                AU  - Xie, Weishun 
                AU  - P.C., Franco Jeen 
                AU  - Liu, Zujun 
                AU  - Tang, Weizhong 
                TI  - Systematic profiling of alternative splicing events and splicing factors in left- and right-sided colon cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102319
                DO  - 10.18632/aging.102319
                SP  - 8270
                EP  - 8293
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Huang, Xiaoliang 
                AU  - Liu, Jungang 
                AU  - Mo, Xianwei 
                AU  - Liu, Haizhou 
                AU  - Wei, Chunyin 
                AU  - Huang, Lingxu 
                AU  - Chen, Jianhong 
                AU  - Tian, Chao 
                AU  - Meng, Yongsheng 
                AU  - Wu, Guo 
                AU  - Xie, Weishun 
                AU  - P.C., Franco Jeen 
                AU  - Liu, Zujun 
                AU  - Tang, Weizhong 
                TI  - Systematic profiling of alternative splicing events and splicing factors in left- and right-sided colon cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102319
                DO  - 10.18632/aging.102319
                SP  - 8270
                EP  - 8293
                PY  - 
                AB  - Left- and right-sided colon cancer (LC and RC) differ substantially in their molecular characteristics and prognoses, and are thus treated using different strategies. We systematically analyzed alternative splicing (AS) events and splicing factors in LC and RC. RNA-seq data were used for genome-wide profiling of AS events that could distinguish LC from RC. The Exon Skip splicing pattern was more common in RC, while the Retained Intron pattern was more common in LC. The AS events that were upregulated in RC were enriched for genes in the axon guidance pathway, while those that were upregulated in LC were enriched for genes in immune-related pathways. Prognostic models based on differentially expressed AS events were built, and a prognostic signature based on these AS events performed well for risk stratification in colon cancer patients. A correlation network of differentially expressed AS events and differentially expressed splicing factors was constructed, and RBM25 was identified as the hub gene in the network. In conclusion, large differences in AS events may contribute to the phenotypic differences between LC and RC. The differentially expressed AS events reported herein could be used as biomarkers and treatment targets for colon cancer.
                ER  -

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

β-arrestin-2 enhances intestinal epithelial apoptosis in necrotizing enterocolitis

Dong Fu, Peng Li, Qingfeng Sheng, Zhibao Lv,

https://doi.org/10.18632/aging.102320 pp 8294—8312

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Fu D, Li P, Sheng Q, Lv Z, . β-arrestin-2 enhances intestinal epithelial apoptosis in necrotizing enterocolitis. . 11:8294-8312. https://doi.org/10.18632/aging.102320

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Fu, Dong 
                AU  - Li, Peng 
                AU  - Sheng, Qingfeng 
                AU  - Lv, Zhibao 
                TI  - β-arrestin-2 enhances intestinal epithelial apoptosis in necrotizing enterocolitis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102320
                DO  - 10.18632/aging.102320
                SP  - 8294
                EP  - 8312
                PY  - 
                AB  - Apoptosis among intestinal epithelial cells contributes to necrotizing enterocolitis (NEC), a severe intestinal disease that particularly affects premature infants. &#x3B2;-arrestin-2, an important regulator of G-protein-coupled receptors, is expressed in intestinal epithelial cells, where its activation promotes apoptosis. We found that &#x3B2;-arrestin-2 was overexpressed in both human and murine NEC samples. &#x3B2;-arrestin-2-deficient mice were protected from endoplasmic reticulum stress and NEC development. The endoplasmic reticulum-resident chaperone BiP was found to promote intestinal epithelial cell survival. Pretreatment of intestinal epithelial cells or mice with the BiP inhibitor HA15 increased cell apoptosis and promoted NEC development. &#x3B2;-arrestin-2 bound to BiP and promoted its polyubiquitination and degradation, thereby facilitating the release of the pro-apoptotic molecule BIK from BiP. Silencing &#x3B2;-arrestin-2 downregulated apoptosis by increasing BiP levels, which suppressed endoplasmic reticulum stress. This study suggests that &#x3B2;-arrestin-2 induces NEC development by inhibiting BiP, thereby triggering apoptosis in response to endoplasmic reticulum stress. Thus, novel therapeutic strategies to inhibit &#x3B2;-arrestin-2 may enhance the treatment of NEC.
                ER  -

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

LncRNAs down-regulate Myh1, Casr, and Mis18a expression in the Substantia Nigra of aged male rats

Guoliang Zhang, Yunxiao Kang, Xu Feng, Rui Cui, Qiqing Guo, Xiaoming Ji, Yuanxiang Huang, Yannan Ma, Shufeng Liu, Geming Shi,

https://doi.org/10.18632/aging.102321 pp 8313—8328

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhang G, Kang Y, Feng X, Cui R, Guo Q, Ji X, Huang Y, Ma Y, Liu S, Shi G, . LncRNAs down-regulate Myh1, Casr, and Mis18a expression in the Substantia Nigra of aged male rats. . 11:8313-8328. https://doi.org/10.18632/aging.102321

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhang, Guoliang 
                AU  - Kang, Yunxiao 
                AU  - Feng, Xu 
                AU  - Cui, Rui 
                AU  - Guo, Qiqing 
                AU  - Ji, Xiaoming 
                AU  - Huang, Yuanxiang 
                AU  - Ma, Yannan 
                AU  - Liu, Shufeng 
                AU  - Shi, Geming 
                TI  - LncRNAs down-regulate Myh1, Casr, and Mis18a expression in the Substantia Nigra of aged male rats
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102321
                DO  - 10.18632/aging.102321
                SP  - 8313
                EP  - 8328
                PY  - 
                AB  - In this study, we used high-throughput RNA sequencing to identify mRNAs, long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) that are differentially expressed in the Substantia Nigra (SN) of aged and young rats. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to perform functional annotation of mRNAs that were either differentially expressed themselves (DEMs), targeted by differentially expressed lncRNAs (DELs), or the parents of differentially expressed circRNAs (DECs). A total of 112 DEMs, 163 DELs, and 98 DECs were found in the SN of aged rats. The down-regulated lncRNA NONRATT010417.2 targeted the down-regulated mRNA Myh1, while the down-regulated lncRNA NONRATT015586.2 and the up-regulated lncRNAs NONRATT000490.2 and NONRATT007029.2 all targeted the down-regulated mRNAs Casr and Mis18a. Western blots and RT-qPCR revealed that Myh1, Casr, and Mis18a protein and mRNA expression were significantly reduced in aged rats compared to young rats. This study improves our understanding of the transcriptional alterations underlying aging-related changes in the SN and provides a foundation for future studies of associated molecular mechanisms.
                ER  -

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

Involvement of adiponectin in age-related increases in tear production in mice

Yosuke Shikama, Mie Kurosawa, Masae Furukawa, Naozumi Ishimaru, Kenji Matsushita,

https://doi.org/10.18632/aging.102322 pp 8329—8346

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Shikama Y, Kurosawa M, Furukawa M, Ishimaru N, Matsushita K, . Involvement of adiponectin in age-related increases in tear production in mice. . 11:8329-8346. https://doi.org/10.18632/aging.102322

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Shikama, Yosuke 
                AU  - Kurosawa, Mie 
                AU  - Furukawa, Masae 
                AU  - Ishimaru, Naozumi 
                AU  - Matsushita, Kenji 
                TI  - Involvement of adiponectin in age-related increases in tear production in mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102322
                DO  - 10.18632/aging.102322
                SP  - 8329
                EP  - 8346
                PY  - 
                AB  - Common age-related changes in the human eye contribute to the development of dry eye, including decreases in aqueous tear production. Although the infiltration of lymphocytes into the lacrimal glands occurs with age, age-related increases in tear production have also been observed in mice; however, the mechanisms underlying this increase remain unclear. We herein demonstrated that increases in tear production were not dependent on body weight gain or systemic conditions, such as insulin resistance, using aged mice and high-fat diet-fed mice. The results obtained also showed that senescence-associated T (SA-T) cells accumulated in the lacrimal glands of aged mice, particularly females. Expression levels of the nuclear transcription factor peroxisome proliferator-activated receptor-&#x3B3; (PPAR&#x3B3;) in whole lacrimal glands and epithelial cells isolated from lacrimal glands were significantly higher in aged mice than in young mice. The expression levels of adiponectin and one of its receptors, AdipoR2, also increased in the lacrimal glands of aged mice, but not in those of high-fat diet-fed mice. Collectively, the present results indicate that PPAR&#x3B3; and adiponectin-mediated signaling contribute to age-related increases in tear production in mice and have potential as therapeutic targets for the treatment of dry eye in humans.
                ER  -

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

Gomisin M2 from Baizuan suppresses breast cancer stem cell proliferation in a zebrafish xenograft model

Yeguo Yang, Erwei Hao, Xianglong Pan, Dechao Tan, Zhengcai Du, Jinling Xie, Xiaotao Hou, Jiagang Deng, Kun Wei,

https://doi.org/10.18632/aging.102323 pp 8347—8361

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Yang Y, Hao E, Pan X, Tan D, Du Z, Xie J, Hou X, Deng J, Wei K, . Gomisin M2 from Baizuan suppresses breast cancer stem cell proliferation in a zebrafish xenograft model. . 11:8347-8361. https://doi.org/10.18632/aging.102323

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Yang, Yeguo 
                AU  - Hao, Erwei 
                AU  - Pan, Xianglong 
                AU  - Tan, Dechao 
                AU  - Du, Zhengcai 
                AU  - Xie, Jinling 
                AU  - Hou, Xiaotao 
                AU  - Deng, Jiagang 
                AU  - Wei, Kun 
                TI  - Gomisin M2 from Baizuan suppresses breast cancer stem cell proliferation in a zebrafish xenograft model
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102323
                DO  - 10.18632/aging.102323
                SP  - 8347
                EP  - 8361
                PY  - 
                AB  - Gomisin M2 isolated from Schisandra viridis A. C. Smith has potential anti-tumor effects on certain cancers, including breast cancer. However, only a few investigations have been conducted on the effects of Gomisin M2 on breast cancer stem cells (CSCs), which have the ability to self-renew and differentiate, as a possible strategy to resolve cancer cell resistance to apoptosis and to improve treatments. It is essential to investigate the effects of Gomisin M2 on breast cancer stem cells (BCSCs). In this study, we enriched breast cancer stem cells with CD44+/CD24- from MDA-MB-231 and HCC1806 cells through magnetic-activated cell sorting and cultured these in serum-free medium. The ability of Gomisin M2 to kill breast cancer stem cells was evaluated in vitro and in vivo. Gomisin M2 significantly inhibited the proliferation of the triple-negative breast cancer cell lines and mammosphere formation in breast CSCs and downregulated the Wnt/&#x3B2;-catenin self-renewal pathway. Moreover, Gomisin M2 induced apoptosis and blocked the mitochondrial membrane potential of BCSCs. Gomisin M2 suppressed the proliferation of MDA-MB-231 and HCC1806 xenografts in zebrafish. Together, these findings suggest that the anti-BCSC activity of Gomisin M2 could become a promising starting point for the discovery of novel BCSC-targeting drugs.
                ER  -

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

Mogroside V protects porcine oocytes from in vitro ageing by reducing oxidative stress through SIRT1 upregulation

Junyu Nie, Lumin Sui, Huiting Zhang, Hengye Zhang, Ke Yan, Xiaogan Yang, Shengsheng Lu, Kehuan Lu, Xingwei Liang,

https://doi.org/10.18632/aging.102324 pp 8362—8373

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Nie J, Sui L, Zhang H, Zhang H, Yan K, Yang X, Lu S, Lu K, Liang X, . Mogroside V protects porcine oocytes from in vitro ageing by reducing oxidative stress through SIRT1 upregulation. . 11:8362-8373. https://doi.org/10.18632/aging.102324

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Nie, Junyu 
 AU - Sui, Lumin 
 AU - Zhang, Huiting 
 AU - Zhang, Hengye 
 AU - Yan, Ke 
 AU - Yang, Xiaogan 
 AU - Lu, Shengsheng 
 AU - Lu, Kehuan 
 AU - Liang, Xingwei 
 TI - Mogroside V protects porcine oocytes from in vitro ageing by reducing oxidative stress through SIRT1 upregulation
 JO - 
 JA - 
 VL - 11
 IS - 19
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102324
 DO - 10.18632/aging.102324
 SP - 8362
 EP - 8373
 PY - 
 AB - Postovulatory ageing compromises oocyte quality and subsequent development in various manners. We aimed to assay the protective effects of mogroside V on porcine oocyte quality during in vitro ageing and explore the related causes. We observed that mogroside V can effectively maintain normal oocyte morphology and early embryo development competence after prolonged culture for 24 h. Moreover, mogroside V can markedly reduce reactive oxygen species (ROS) levels, alleviate spindle formation and chromosome alignment abnormalities, improve mitochondrial contents, adenosine triphosphate (ATP) levels and the membrane potential (&#x394;&#x3A8;m), and reduce early apoptosis in aged oocytes. We examined the molecular changes and found that SIRT1 expression was decreased in in vitro aged oocytes but was maintained by exposure to mogroside V. However, when SIRT1 was successfully inhibited by the specific inhibitor EX-527, mogroside V could not reduce ROS levels or alleviate abnormal spindle organization and chromosome misalignment. In summary, our results demonstrated that mogroside V can alleviate the deterioration of oocyte quality during in vitro ageing, possibly by reducing oxidative stress through SIRT1 upregulation.
 ER -

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

LncRNA TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the miR-134-5p/MBTD1 axis

Dong Fu, Chunwen Lu, Xingzhou Qu, Peng Li, Kai Chen, Liancheng Shan, Xiaodong Zhu,

https://doi.org/10.18632/aging.102325 pp 8374—8385

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Fu D, Lu C, Qu X, Li P, Chen K, Shan L, Zhu X, . LncRNA TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the miR-134-5p/MBTD1 axis. . 11:8374-8385. https://doi.org/10.18632/aging.102325

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Fu, Dong 
                AU  - Lu, Chunwen 
                AU  - Qu, Xingzhou 
                AU  - Li, Peng 
                AU  - Chen, Kai 
                AU  - Shan, Liancheng 
                AU  - Zhu, Xiaodong 
                TI  - LncRNA TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the miR-134-5p/MBTD1 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102325
                DO  - 10.18632/aging.102325
                SP  - 8374
                EP  - 8385
                PY  - 
                AB  - Aim: To explore the mechanism by which long non-coding RNA (lncRNA) TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the microRNA miR-134-5p/malignant brain tumour domain containing 1 (MBTD1) axis.Results: The lncRNA TTN-AS1 was highly expressed in osteosarcoma and was associated with poor prognosis. The lncRNA TTN-AS1 promoted cell viability and inhibited apoptosis. MiR-134-5p targeted MBTD1, which was regulated by lncRNA TTN-AS1. MBTD1 was highly expressed in osteosarcoma and was associated with poor prognosis. MBTD1 promoted cell viability and inhibited apoptosis, and knockdown of MBTD1 reversed the cancer-promoting effects of lncRNA TTN-AS1. Downregulation of lncRNA TTN-AS1 reduced drug resistance.Conclusion: In osteosarcoma, lncRNA TTN-AS1 promoted the expression of MBTD1 by targeting miR-134-5p and regulated cell growth, apoptosis and drug resistance.Methods: The expression characteristics of genes in osteosarcoma patients were analysed using bioinformatics. Plasmid transfection technology was applied to silence or overexpress lncRNA TTN-AS1, miR-134-5p and MBTD1. Western blotting and quantitative polymerase chain reaction (qPCR) were used to detect protein and RNA, respectively. A cell counting kit 8 (CCK-8) and flow cytometry were used to detect cell viability and apoptosis. The effects of lncRNA TTN-AS1 and MBTD1 on osteosarcoma in vivo were studied by using a tumour burden assay.
                ER  -

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

Cognitive impairment and transcriptomic profile in hippocampus of young mice after multiple neonatal exposures to sevoflurane

Shao-Yong Song, Xiao-Wen Meng, ZhengYuan Xia, Hong Liu, Juan Zhang, Qing-Cai Chen, Hua-Yue Liu, Fu-Hai Ji, Ke Peng,

https://doi.org/10.18632/aging.102326 pp 8386—8417

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Song S, Meng X, Xia Z, Liu H, Zhang J, Chen Q, Liu H, Ji F, Peng K, . Cognitive impairment and transcriptomic profile in hippocampus of young mice after multiple neonatal exposures to sevoflurane. . 11:8386-8417. https://doi.org/10.18632/aging.102326

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Song, Shao-Yong 
                AU  - Meng, Xiao-Wen 
                AU  - Xia, ZhengYuan 
                AU  - Liu, Hong 
                AU  - Zhang, Juan 
                AU  - Chen, Qing-Cai 
                AU  - Liu, Hua-Yue 
                AU  - Ji, Fu-Hai 
                AU  - Peng, Ke 
                TI  - Cognitive impairment and transcriptomic profile in hippocampus of young mice after multiple neonatal exposures to sevoflurane
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102326
                DO  - 10.18632/aging.102326
                SP  - 8386
                EP  - 8417
                PY  - 
                AB  - Children with repeated inhalational anesthesia may develop cognitive disorders. This study aimed to investigate the transcriptome-wide response of hippocampus in young mice that had been exposed to multiple sevoflurane in the neonatal period. Mice received 3% sevoflurane for 2 h on postnatal day (PND) 6, 8, and 10, followed by arterial blood gas test on PND 10, behavioral experiments on PND 31&#x2013;36, and RNA sequencing (RNA-seq) of hippocampus on PND 37. Functional annotation and protein-protein interaction analyses of differentially expressed genes (DEGs) and quantitative reverse transcription polymerase chain reaction (qPCR) were performed. Neonatal sevoflurane exposures induced cognitive and social behavior disorders in young mice. RNA-seq identified a total of 314 DEGs. Several enriched biological processes (ion channels, brain development, learning, and memory) and signaling pathways (oxytocin signaling pathway and glutamatergic, cholinergic, and GABAergic synapses) were highlighted. As hub-proteins, Pten was involved in nervous system development, synapse assembly, learning, memory, and behaviors, Nos3 and Pik3cd in oxytocin signaling pathway, and Cdk16 in exocytosis and phosphorylation. Some top DEGs were validated by qPCR. This study revealed a transcriptome-wide profile in mice hippocampus after multiple neonatal exposures to sevoflurane, promoting better understanding of underlying mechanisms and investigation of preventive strategies.
                ER  -

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

mTORC1-Sch9 regulates hydrogen sulfide production through the transsulfuration pathway

Zhou Lyu, Xuejie Gao, Weiyan Wang, Jinye Dang, Li Yang, Mengli Yan, Shah Arman Ali, Yang Liu, Binghua Liu, Meng Yu, Linfang Du, Ke Liu,

https://doi.org/10.18632/aging.102327 pp 8418—8432

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lyu Z, Gao X, Wang W, Dang J, Yang L, Yan M, Ali SA, Liu Y, Liu B, Yu M, Du L, Liu K, . mTORC1-Sch9 regulates hydrogen sulfide production through the transsulfuration pathway. . 11:8418-8432. https://doi.org/10.18632/aging.102327

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lyu, Zhou 
                AU  - Gao, Xuejie 
                AU  - Wang, Weiyan 
                AU  - Dang, Jinye 
                AU  - Yang, Li 
                AU  - Yan, Mengli 
                AU  - Ali, Shah Arman 
                AU  - Liu, Yang 
                AU  - Liu, Binghua 
                AU  - Yu, Meng 
                AU  - Du, Linfang 
                AU  - Liu, Ke 
                TI  - mTORC1-Sch9 regulates hydrogen sulfide production through the transsulfuration pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102327
                DO  - 10.18632/aging.102327
                SP  - 8418
                EP  - 8432
                PY  - 
                AB  - Endogenous hydrogen sulfide mediates anti-aging benefits of dietary restriction (DR). However, it is unclear how H2S production is regulated by pathways related to DR. Due to the importance of mTORC1 pathway in DR, we investigated the effects of Sch9, a yeast homolog of mammalian S6K1 and a major substrate of mTORC1 on H2S production in yeast Saccharomyces cerevisiae. We found that inhibition of the mTORC1-Sch9 pathway by SCH9 deletion, rapamycin or myriocin treatment resulted in a dramatic decrease in H2S production. Although deficiency of SCH9 did not alter the intracellular level of methionine, the intracellular level of cysteine increased in &#x394;sch9 cells. The expression of CYS3 and CYS4, two transsulfuration pathway genes encoding cystathionine gamma-lyase (CGL) and cystathionine beta-synthase (CBS), were also decreased under mTORC1-Sch9 inhibition. Overexpression of CYS3 or CYS4 in &#x394;sch9 cells or WT cells treated with rapamycin rescued the deficiency of H2S production. Finally, we also observed a reduction in H2S production and lowering of both mRNA and protein levels of CGL and CBS in cultured human cells treated with rapamycin to reduce mTORC1 pathway activity. Thus, our findings reveal a probably conserved mechanism in which H2S production by the transsulfuration pathway is regulated by mTORC1-Sch9 signaling.
                ER  -

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

Brain pyrimidine nucleotide synthesis and Alzheimer disease

Alba Pesini, Eldris Iglesias, M.Pilar Bayona-Bafaluy, Nuria Garrido-Pérez, Patricia Meade, Paula Gaudó, Irene Jiménez-Salvador, Pol Andrés-Benito, Julio Montoya, Isidro Ferrer, Pedro Pesini, Eduardo Ruiz-Pesini,

https://doi.org/10.18632/aging.102328 pp 8433—8462

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Pesini A, Iglesias E, Bayona-Bafaluy M, Garrido-Pérez N, Meade P, Gaudó P, Jiménez-Salvador I, Andrés-Benito P, Montoya J, Ferrer I, Pesini P, Ruiz-Pesini E, . Brain pyrimidine nucleotide synthesis and Alzheimer disease. . 11:8433-8462. https://doi.org/10.18632/aging.102328

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Pesini, Alba 
                AU  - Iglesias, Eldris 
                AU  - Bayona-Bafaluy, M.Pilar 
                AU  - Garrido-Pérez, Nuria 
                AU  - Meade, Patricia 
                AU  - Gaudó, Paula 
                AU  - Jiménez-Salvador, Irene 
                AU  - Andrés-Benito, Pol 
                AU  - Montoya, Julio 
                AU  - Ferrer, Isidro 
                AU  - Pesini, Pedro 
                AU  - Ruiz-Pesini, Eduardo 
                TI  - Brain pyrimidine nucleotide synthesis and Alzheimer disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102328
                DO  - 10.18632/aging.102328
                SP  - 8433
                EP  - 8462
                PY  - 
                AB  - Many patients suffering late-onset Alzheimer disease show a deficit in respiratory complex IV activity. The de novo pyrimidine biosynthesis pathway connects with the mitochondrial respiratory chain upstream from respiratory complex IV. We hypothesized that these patients would have decreased pyrimidine nucleotide levels. Then, different cell processes for which these compounds are essential, such as neuronal membrane generation and maintenance and synapses production, would be compromised. Using a cell model, we show that inhibiting oxidative phosphorylation function reduces neuronal differentiation. Linking these processes to pyrimidine nucleotides, uridine treatment recovers neuronal differentiation. To unmask the importance of these pathways in Alzheimer disease, we firstly confirm the existence of the de novo pyrimidine biosynthesis pathway in adult human brain. Then, we report altered mRNA levels for genes from both de novo pyrimidine biosynthesis and pyrimidine salvage pathways in brain from patients with Alzheimer disease. Thus, uridine supplementation might be used as a therapy for those Alzheimer disease patients with low respiratory complex IV activity.
                ER  -

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

Effect of age as a continuous variable on survival outcomes and treatment selection in patients with extranodal nasal-type NK/T-cell lymphoma from the China Lymphoma Collaborative Group (CLCG)

Wei-Xin Liu, Mei Shi, Hang Su, Ying Wang, Xia He, Li-Ming Xu, Zhi-Yong Yuan, Li-Ling Zhang, Gang Wu, Bao-Lin Qu, Li-Ting Qian, Xiao-Rong Hou, Fu-Quan Zhang, Yu-Jing Zhang, Yuan Zhu, Jian-Zhong Cao, Sheng-Min Lan, Jun-Xin Wu, Tao Wu, Su-Yu Zhu, Shu-Nan Qi, Yong Yang, Bo Chen, Ye-Xiong Li,

https://doi.org/10.18632/aging.102331 pp 8463—8473

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liu W, Shi M, Su H, Wang Y, He X, Xu L, Yuan Z, Zhang L, Wu G, Qu B, Qian L, Hou X, Zhang F, et al, . Effect of age as a continuous variable on survival outcomes and treatment selection in patients with extranodal nasal-type NK/T-cell lymphoma from the China Lymphoma Collaborative Group (CLCG). . 11:8463-8473. https://doi.org/10.18632/aging.102331

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liu, Wei-Xin 
                AU  - Shi, Mei 
                AU  - Su, Hang 
                AU  - Wang, Ying 
                AU  - He, Xia 
                AU  - Xu, Li-Ming 
                AU  - Yuan, Zhi-Yong 
                AU  - Zhang, Li-Ling 
                AU  - Wu, Gang 
                AU  - Qu, Bao-Lin 
                AU  - Qian, Li-Ting 
                AU  - Hou, Xiao-Rong 
                AU  - Zhang, Fu-Quan 
                AU  - Zhang, Yu-Jing 
                AU  - Zhu, Yuan 
                AU  - Cao, Jian-Zhong 
                AU  - Lan, Sheng-Min 
                AU  - Wu, Jun-Xin 
                AU  - Wu, Tao 
                AU  - Zhu, Su-Yu 
                AU  - Qi, Shu-Nan 
                AU  - Yang, Yong 
                AU  - Chen, Bo 
                AU  - Li, Ye-Xiong 
                TI  - Effect of age as a continuous variable on survival outcomes and treatment selection in patients with extranodal nasal-type NK/T-cell lymphoma from the China Lymphoma Collaborative Group (CLCG)
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102331
                DO  - 10.18632/aging.102331
                SP  - 8463
                EP  - 8473
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Liu, Wei-Xin 
                AU  - Shi, Mei 
                AU  - Su, Hang 
                AU  - Wang, Ying 
                AU  - He, Xia 
                AU  - Xu, Li-Ming 
                AU  - Yuan, Zhi-Yong 
                AU  - Zhang, Li-Ling 
                AU  - Wu, Gang 
                AU  - Qu, Bao-Lin 
                AU  - Qian, Li-Ting 
                AU  - Hou, Xiao-Rong 
                AU  - Zhang, Fu-Quan 
                AU  - Zhang, Yu-Jing 
                AU  - Zhu, Yuan 
                AU  - Cao, Jian-Zhong 
                AU  - Lan, Sheng-Min 
                AU  - Wu, Jun-Xin 
                AU  - Wu, Tao 
                AU  - Zhu, Su-Yu 
                AU  - Qi, Shu-Nan 
                AU  - Yang, Yong 
                AU  - Chen, Bo 
                AU  - Li, Ye-Xiong 
                TI  - Effect of age as a continuous variable on survival outcomes and treatment selection in patients with extranodal nasal-type NK/T-cell lymphoma from the China Lymphoma Collaborative Group (CLCG)
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102331
                DO  - 10.18632/aging.102331
                SP  - 8463
                EP  - 8473
                PY  - 
                AB  - Purpose: The aim of this study was to determine the impact of analyzing age as a continuous variable on survival outcomes and treatment selection for extranodal nasal-type NK/T-cell lymphoma.Results: The risk of mortality increased with increasing age, without an apparent cutoff point. Patients&#x2019; age, as a continuous variable, was independently associated with overall survival after adjustment for covariates. Older early-stage patients were more likely to receive radiotherapy only whereas young-adult advanced-stage patients tended to receive non-anthracycline-based chemotherapy. A decreased risk of mortality with radiotherapy versus chemotherapy only in early-stage patients (HR, 0.347, P &lt; 0.001) or non-anthracycline-based versus anthracycline-based chemotherapy in early-stage (HR, 0.690, P = 0.001) and advanced-stage patients (HR, 0.678, P = 0.045) was maintained in patients of all ages.Conclusions: These findings support making treatment decisions based on disease-related risk factors rather than dichotomized chronological age.Patients and Methods: Data on 2640 patients with extranodal nasal-type NK/T-cell lymphoma from the China Lymphoma Collaborative Group database were analyzed retrospectively. Age as a continuous variable was entered into the Cox regression model using penalized spline analysis to determine the association of age with overall survival (OS) and treatment benefits.
                ER  -

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

The prognostic value of major facilitator superfamily domain-containing protein 2A in patients with hepatocellular carcinoma

Shan Xing, Jun Kan, Aishan Su, Qiao-Dan Liu, Kailin Wang, Xiuyu Cai, Jun Dong,

https://doi.org/10.18632/aging.102333 pp 8474—8483

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xing S, Kan J, Su A, Liu Q, Wang K, Cai X, Dong J, . The prognostic value of major facilitator superfamily domain-containing protein 2A in patients with hepatocellular carcinoma. . 11:8474-8483. https://doi.org/10.18632/aging.102333

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Xing, Shan 
                AU  - Kan, Jun 
                AU  - Su, Aishan 
                AU  - Liu, Qiao-Dan 
                AU  - Wang, Kailin 
                AU  - Cai, Xiuyu 
                AU  - Dong, Jun 
                TI  - The prognostic value of major facilitator superfamily domain-containing protein 2A in patients with hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102333
                DO  - 10.18632/aging.102333
                SP  - 8474
                EP  - 8483
                PY  - 
                AB  - Introduction: We aimed to characterize the expression of major facilitator superfamily domain-containing protein 2A (MFSD2A) in hepatocellular carcinoma (HCC) patients and analyze its prognostic value.Results: Immunohistochemistry revealed that low expression of MFSD2A was present in 37 of 79 cases (46.84%), which was significantly correlated with poor histological differentiation (P = 0.012). The plasma MFSD2A level in HCC patients was significantly lower than in healthy controls (P = 0.0079) and controls with chronic hepatitis B virus (HBV) infection (P = 0.0430). Moreover, patients with lower MFSD2A expression had shorter survival than higher expression (P = 0.021). Multivariate analysis revealed that MFSD2A was an independent prognostic predictor for HCC patients (P = 0.027).Conclusion: The current study indicate MFSD2A may be an optimal diagnostic and prognostic biomarker for HCC.Methods: First, we examined MFSD2A expression in 24 paired HCC and nontumorous tissues by real-time quantitative PCR (RT-qPCR). Second, the protein levels of MFSD2A in 11 paired HCC and nontumorous tissues were investigated by western blotting (WB). Moreover, MFSD2A protein expression was evaluated by immunohistochemistry in 79 HCC patients. In addition, we detected the plasma level of MFSD2A in HCC patients and healthy individuals and investigated the relationship between MFSD2A expression and clinicopathological parameters or prognosis of HCC patients.
                ER  -

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

CircUBAP2-mediated competing endogenous RNA network modulates tumorigenesis in pancreatic adenocarcinoma

Rongjie Zhao, Junjie Ni, Si Lu, Sujing Jiang, Liangkun You, Hao Liu, Jiawei Shou, Chongya Zhai, Wei Zhang, Shengpeng Shao, Xinmei Yang, Hongming Pan, Weidong Han,

https://doi.org/10.18632/aging.102334 pp 8484—8501

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhao R, Ni J, Lu S, Jiang S, You L, Liu H, Shou J, Zhai C, Zhang W, Shao S, Yang X, Pan H, Han W, . CircUBAP2-mediated competing endogenous RNA network modulates tumorigenesis in pancreatic adenocarcinoma. . 11:8484-8501. https://doi.org/10.18632/aging.102334

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhao, Rongjie 
                AU  - Ni, Junjie 
                AU  - Lu, Si 
                AU  - Jiang, Sujing 
                AU  - You, Liangkun 
                AU  - Liu, Hao 
                AU  - Shou, Jiawei 
                AU  - Zhai, Chongya 
                AU  - Zhang, Wei 
                AU  - Shao, Shengpeng 
                AU  - Yang, Xinmei 
                AU  - Pan, Hongming 
                AU  - Han, Weidong 
                TI  - CircUBAP2-mediated competing endogenous RNA network modulates tumorigenesis in pancreatic adenocarcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102334
                DO  - 10.18632/aging.102334
                SP  - 8484
                EP  - 8501
                PY  - 
                AB  - We investigated the role of the competing endogenous RNA (ceRNA) network in the development and progression of pancreatic adenocarcinoma (PAAD). We analyzed the expression profiles of PAAD and normal pancreatic tissues from multiple GEO databases and identified 457 differentially expressed circular RNAs (DEcircRNAs), 19 microRNAs (DEmiRNAs) and 1993 mRNAs (DEmRNAs). We constructed a ceRNA network consisting of 4 DEcircRNAs, 3 DEmiRNAs and 149 DEmRNAs that regulates the NF-kappa B, PI3K-Akt, and Wnt signaling pathways. We then identified and validated five hub genes, CXCR4, HIF1A, ZEB1, SDC1 and TWIST1, which are overexpressed in PAAD tissues. The expression of CXCR4, HIF1A, ZEB1, and SDC1 in PAAD was regulated by circ-UBAP2 and hsa-miR-494. The expression of CXCR4 and ZEB1 correlated with the levels of M2 macrophages, T-regulatory cells (Tregs) and exhausted T cells in the PAAD tissues. The expression of CXCR4 and ZEB1 positively correlated with the expression of CTLA-4 and PD-1. This suggests that CXCR4 and ZEB1 proteins inhibit antigen presentation and promote immune escape mechanisms in PAAD cells. In summary, our data suggest that the circUBAP2-mediated ceRNA network modulates PAAD by regulating the infiltration and function of immune cells.
                ER  -

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

Albumin infusion may decrease the incidence and severity of overt hepatic encephalopathy in liver cirrhosis

Zhaohui Bai, Mauro Bernardi, Eric M. Yoshida, Hongyu Li, Xiaozhong Guo, Nahum Méndez-Sánchez, Yingying Li, Ran Wang, Jiao Deng, Xingshun Qi,

https://doi.org/10.18632/aging.102335 pp 8502—8525

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Bai Z, Bernardi M, Yoshida EM, Li H, Guo X, Méndez-Sánchez N, Li Y, Wang R, Deng J, Qi X, . Albumin infusion may decrease the incidence and severity of overt hepatic encephalopathy in liver cirrhosis. . 11:8502-8525. https://doi.org/10.18632/aging.102335

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Bai, Zhaohui 
                AU  - Bernardi, Mauro 
                AU  - Yoshida, Eric M. 
                AU  - Li, Hongyu 
                AU  - Guo, Xiaozhong 
                AU  - Méndez-Sánchez, Nahum 
                AU  - Li, Yingying 
                AU  - Wang, Ran 
                AU  - Deng, Jiao 
                AU  - Qi, Xingshun 
                TI  - Albumin infusion may decrease the incidence and severity of overt hepatic encephalopathy in liver cirrhosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102335
                DO  - 10.18632/aging.102335
                SP  - 8502
                EP  - 8525
                PY  - 
                AB  - Background: The role of human albumin infusion for the prevention and treatment of overt hepatic encephalopathy (HE) in liver cirrhosis remains unclear.
Results: Among the 708 patients without pre-existing overt HE, albumin infusion significantly decreased the incidence of overt HE (4.20% versus 12.70%, P&lt;0.001) and in-hospital mortality (1.70% versus 5.40%, P=0.008). Among the 182 patients with overt HE at admission or during hospitalization, albumin infusion significantly improved overt HE (84.60% versus 68.10%, P=0.009) and decreased in-hospital mortality (7.70% versus 19.80%, P=0.018). Meta-analysis of 6 studies found that albumin infusion might decrease the risk of overt HE (OR=1.63, P=0.07), but the difference was not statistically significant. Meta-analysis of 3 studies found that albumin infusion significantly improved overt HE (OR=2.40, P=0.04).
Conclusions: Based on the results of our retrospective study and meta-analysis, albumin infusion might prevent from the occurrence of overt HE and improve the severity of overt HE in cirrhosis. Our retrospective study also suggested that albumin infusion improved the outcomes of cirrhotic patients regardless of overt HE.
Methods: Cirrhotic patients consecutively admitted between January 2010 and June 2014 were considered in a retrospective study. A 1:1 propensity score matching analysis was performed. Additionally, publications regarding albumin infusion for the management of overt HE were systematically searched. Meta-analyses were performed by random-effect model. Odds ratio (OR) was calculated.
                ER  -

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

Ninjurin 2 overexpression promotes human colorectal cancer cell growth in vitro and in vivo

Gang Li, Li-Na Zhou, Han Yang, Xixi He, Yuxia Duan, Fang Wu,

https://doi.org/10.18632/aging.102336 pp 8526—8541

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li G, Zhou L, Yang H, He X, Duan Y, Wu F, . Ninjurin 2 overexpression promotes human colorectal cancer cell growth in vitro and in vivo. . 11:8526-8541. https://doi.org/10.18632/aging.102336

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Li, Gang 
 AU - Zhou, Li-Na 
 AU - Yang, Han 
 AU - He, Xixi 
 AU - Duan, Yuxia 
 AU - Wu, Fang 
 TI - Ninjurin 2 overexpression promotes human colorectal cancer cell growth in vitro and in vivo
 JO - 
 JA - 
 VL - 11
 IS - 19
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102336
 DO - 10.18632/aging.102336
 SP - 8526
 EP - 8541
 PY - 
 AB - Ninjurin 2 (NINJ2) is a novel adhesion molecule. Its expression and potential function in human colorectal cancer (CRC) cells are studied. We show that NINJ2 is overexpressed in established (HT-29) and primary CRC cells and in human colon cancer tissues. Its expression level is low in colon epithelial cells and normal colon tissues. NINJ2 shRNA or knockout (by CRSIPR/Cas9) potently inhibited human CRC cell survival and proliferation, while significantly inducing cell apoptosis. Conversely, lentivirus-mediated NINJ2 overexpression promoted CRC cell proliferation. NINJ2 co-immunoprecipitated with multiple RTKs (EGFR, PDGFR&#x3B1;/&#x3B2; and FGFR) in CRC cells and human colon cancer tissues. In HT-29 cells, RTKs&#x2019; downstream signalings, Akt and Erk, were significantly inhibited by NINJ2 shRNA or knockout, but augmented following ectopic NINJ2 overexpression. In vivo, NINJ2-silenced or NINJ2-knockout CRC xenografts grew significantly slower than the control xenografts. Akt-Erk activation was largely inhibited in CRC xenografts with NINJ2 silencing or knockout. Taken together, NINJ2 overexpression promotes CRC cell growth in vitro and in vivo.
 ER -

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

Probucol, a “non-statin” cholesterol-lowering drug, ameliorates D-galactose induced cognitive deficits by alleviating oxidative stress via Keap1/Nrf2 signaling pathway in mice

Jin-Lan Huang, Chao Yu, Min Su, Si-Man Yang, Fan Zhang, Yuan-Yuan Chen, Jin-Yuan Liu, Yi-Fan Jiang, Zhen-Guo Zhong, Deng-Pan Wu,

https://doi.org/10.18632/aging.102337 pp 8542—8555

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Huang J, Yu C, Su M, Yang S, Zhang F, Chen Y, Liu J, Jiang Y, Zhong Z, Wu D, . Probucol, a “non-statin” cholesterol-lowering drug, ameliorates D-galactose induced cognitive deficits by alleviating oxidative stress via Keap1/Nrf2 signaling pathway in mice. . 11:8542-8555. https://doi.org/10.18632/aging.102337

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Huang, Jin-Lan 
                AU  - Yu, Chao 
                AU  - Su, Min 
                AU  - Yang, Si-Man 
                AU  - Zhang, Fan 
                AU  - Chen, Yuan-Yuan 
                AU  - Liu, Jin-Yuan 
                AU  - Jiang, Yi-Fan 
                AU  - Zhong, Zhen-Guo 
                AU  - Wu, Deng-Pan 
                TI  - Probucol, a “non-statin” cholesterol-lowering drug, ameliorates D-galactose induced cognitive deficits by alleviating oxidative stress via Keap1/Nrf2 signaling pathway in mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102337
                DO  - 10.18632/aging.102337
                SP  - 8542
                EP  - 8555
                PY  - 
                AB  - Oxidative stress plays a vital role in the initiation and progression of age-related neurodegenerative diseases. Ameliorating oxidative damage is therefore considered as a beneficial strategy for the treatment of age-related neurodegenerative disorders. Probucol (Prob), a lipid-lowering prototype agent, was reported to treat cardiovascular diseases, chronic kidney disease and diabetes mellitus. However, whether Prob has an effect on age-related neurodegenerative diseases remains unknown. In the study, it was found that Prob ameliorated D-galactose (D-gal) induced cognitive deficits and neuronal loss in the hippocampal CA1 region. Moreover, Prob alleviated ROS and MDA levels by elevating SOD, GSH-PX and HO-1 mRNA and protein expressions, and improving plasmic and cerebral SOD and GSH-PX activities in D-gal treated mice. Furthermore, Prob promoted the dissociation of Keap1/Nrf2 complex leading to the accumulation of Nrf2 in nucleus, implying that the improved anti-oxidant property of Prob is mediated by Keap1/Nrf2 pathway. The study firstly demonstrates the favorable effects of Prob against cognitive impairments in a senescent mouse model, rendering this compound a promising agent for the treatment or prevention of age-related neurodegenerative disease.
                ER  -

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

Conserved aging-related signatures of senescence and inflammation in different tissues and species

Emanuel Barth, Akash Srivastava, Milan Stojiljkovic, Christiane Frahm, Hubertus Axer, Otto W. Witte, Manja Marz,

https://doi.org/10.18632/aging.102345 pp 8556—8572

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Barth E, Srivastava A, Stojiljkovic M, Frahm C, Axer H, Witte OW, Marz M, . Conserved aging-related signatures of senescence and inflammation in different tissues and species. . 11:8556-8572. https://doi.org/10.18632/aging.102345

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Barth, Emanuel 
                AU  - Srivastava, Akash 
                AU  - Stojiljkovic, Milan 
                AU  - Frahm, Christiane 
                AU  - Axer, Hubertus 
                AU  - Witte, Otto W. 
                AU  - Marz, Manja 
                TI  - Conserved aging-related signatures of senescence and inflammation in different tissues and species
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102345
                DO  - 10.18632/aging.102345
                SP  - 8556
                EP  - 8572
                PY  - 
                AB  - Increasing evidence indicates that chronic inflammation and senescence are the cause of many severe age-related diseases, with both biological processes highly upregulated during aging. However, until now, it has remained unknown whether specific inflammation- or senescence-related genes exist that are common between different species or tissues. These potential markers of aging could help to identify possible targets for therapeutic interventions of aging-associated afflictions and might also deepen our understanding of the principal mechanisms of aging. With the objective of identifying such signatures of aging and tissue-specific aging markers, we analyzed a multitude of cross-sectional RNA-Seq data from four evolutionarily distinct species (human, mouse and two fish) and four different tissues (blood, brain, liver and skin). In at least three different species and three different tissues, we identified several genes that displayed similar expression patterns that might serve as potential aging markers. Additionally, we show that genes involved in aging-related processes tend to be tighter controlled in long-lived than in average-lived individuals. These observations hint at a general genetic level that affect an individual&#x2019;s life span. Altogether, this descriptive study contributes to a better understanding of common aging signatures as well as tissue-specific aging patterns and supplies the basis for further investigative age-related studies.
                ER  -

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

High body mass index, brain metabolism and connectivity: an unfavorable effect in elderly females

Arianna Sala, Maura Malpetti, Anna Ferrulli, Luigi Gianolli, Livio Luzi, Daniela Perani, Alzheimer’s Disease Neuroimaging Initiative (ADNI) database,

https://doi.org/10.18632/aging.102347 pp 8573—8586

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Sala A, Malpetti M, Ferrulli A, Gianolli L, Luzi L, Perani D, , . High body mass index, brain metabolism and connectivity: an unfavorable effect in elderly females. . 11:8573-8586. https://doi.org/10.18632/aging.102347

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Sala, Arianna 
                AU  - Malpetti, Maura 
                AU  - Ferrulli, Anna 
                AU  - Gianolli, Luigi 
                AU  - Luzi, Livio 
                AU  - Perani, Daniela 
                AU  - ,  
                TI  - High body mass index, brain metabolism and connectivity: an unfavorable effect in elderly females
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102347
                DO  - 10.18632/aging.102347
                SP  - 8573
                EP  - 8586
                PY  - 
                AB  - There are reported gender differences in brain connectivity associated with obesity. In the elderlies, the neural endophenotypes of obesity are yet to be elucidated. We aim at exploring the brain metabolic and connectivity correlates to different BMI levels in elderly individuals, taking into account gender as variable of interest.We evaluated the association between BMI, brain metabolism and connectivity, in elderly females and males, by retrospectively collecting a large cohort of healthy elderly subjects (N=222; age=74.03&#xB1;5.88 [61.2-85.9] years; M/F=115/107; BMI=27.00&#xB1;4.02 [19.21-38.79] kg/m2). Subjects underwent positron emission tomography with [18F]FDG. We found that, in females, high BMI was associated with increased brain metabolism in the orbitofrontal cortex (R=0.44; p&lt;0.001). A significant BMI-by-gender interaction was present (F=7.024, p=0.009). We also revealed an altered connectivity seeding from these orbitofrontal regions, namely expressing as a decreased connectivity in crucial control/decision making circuits, and as an abnormally elevated connectivity in reward circuits, only in females. Our findings support a link between high BMI and altered brain metabolism and neural connectivity, only in elderly females. These findings indicate a strong gender effect of high BMI and obesity that brings to considerations for medical practice and health policy.
                ER  -

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

A molecular sub-cluster of colon cancer cells with low VDR expression is sensitive to chemotherapy, BRAF inhibitors and PI3K-mTOR inhibitors treatment

Haiwei Wang, Xinrui Wang, Liangpu Xu, Ji Zhang, Hua Cao,

https://doi.org/10.18632/aging.102349 pp 8587—8603

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang H, Wang X, Xu L, Zhang J, Cao H, . A molecular sub-cluster of colon cancer cells with low VDR expression is sensitive to chemotherapy, BRAF inhibitors and PI3K-mTOR inhibitors treatment. . 11:8587-8603. https://doi.org/10.18632/aging.102349

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Haiwei 
                AU  - Wang, Xinrui 
                AU  - Xu, Liangpu 
                AU  - Zhang, Ji 
                AU  - Cao, Hua 
                TI  - A molecular sub-cluster of colon cancer cells with low VDR expression is sensitive to chemotherapy, BRAF inhibitors and PI3K-mTOR inhibitors treatment
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102349
                DO  - 10.18632/aging.102349
                SP  - 8587
                EP  - 8603
                PY  - 
                AB  - Gene expression based consensus molecular subtypes (CMS) and non-negative matrix factorization (NMF) sub-clusters are robust colon cancer classification systems. Although, the molecular features are clear, colon cancer subgroups based interventions are limited. To address this problem, we analyze the CMS and NMF subgroup guided drug sensitivity in colon cancer cell lines. CMS3 subtype cells are sensitive to 5-Fluorouracil, while, CMS4 subtype cells are sensitive to cisplatin treatment. In NMF classification, a sub-cluster is specifically sensitive to chemotherapy, BRAF inhibitors, PI3K-mTOR inhibitors and NOTCH inhibitor treatment. This sub-cluster has low frequency of TP53, POLE, PIK3CA and BRAF mutation. Transcriptional analysis demonstrates low NOTCH signaling activity, low CDX2 and VDR expression in this sub-cluster. CDX2 and VDR are significantly associated with the sensitivity of chemotherapy, BRAF inhibitors and PI3K-mTOR inhibitors. Moreover, a positive correlation between VDR and CDX2 is identified. VDR and CDX2 mediated regulatory networks are constructed. At last, three or four sub-clusters classification is validated in colon cancer patients. Overall, our results suggest a molecular sub-cluster of colon cancer cells with low CDX2 and VDR expression is sensitive to chemotherapy, BRAF inhibitors and PI3K-mTOR inhibitors treatment and provide an example of translation of cancer classification to subgroup guided therapies.
                ER  -

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

Tryptophan metabolite 5-methoxytryptophan ameliorates arterial denudation-induced intimal hyperplasia via opposing effects on vascular endothelial and smooth muscle cells

Chung-Huang Chen, Yen-Chun Ho, Hua-Hui Ho, Li-Yu Liang, Wei-Cheng Jiang, Guan-Lin Lee, Jen-Kuang Lee, Yu-Juei Hsu, Cheng-Chin Kuo, Kenneth K. Wu, Shaw-Fang Yet,

https://doi.org/10.18632/aging.102350 pp 8604—8622

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen C, Ho Y, Ho H, Liang L, Jiang W, Lee G, Lee J, Hsu Y, Kuo C, Wu KK, Yet S, . Tryptophan metabolite 5-methoxytryptophan ameliorates arterial denudation-induced intimal hyperplasia via opposing effects on vascular endothelial and smooth muscle cells. . 11:8604-8622. https://doi.org/10.18632/aging.102350

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Chung-Huang 
                AU  - Ho, Yen-Chun 
                AU  - Ho, Hua-Hui 
                AU  - Liang, Li-Yu 
                AU  - Jiang, Wei-Cheng 
                AU  - Lee, Guan-Lin 
                AU  - Lee, Jen-Kuang 
                AU  - Hsu, Yu-Juei 
                AU  - Kuo, Cheng-Chin 
                AU  - Wu, Kenneth K. 
                AU  - Yet, Shaw-Fang 
                TI  - Tryptophan metabolite 5-methoxytryptophan ameliorates arterial denudation-induced intimal hyperplasia via opposing effects on vascular endothelial and smooth muscle cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102350
                DO  - 10.18632/aging.102350
                SP  - 8604
                EP  - 8622
                PY  - 
                AB  - Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide, particularly among older adults. Despite the advent of medical technology, restenosis is still an issue after interventional procedures. Tryptophan metabolite 5-methoxytryptophan (5-MTP) has recently been shown to protect against systemic inflammatory responses. This study aimed to investigate the function and mechanisms of 5-MTP in interventional procedure-induced restenosis. We found that after mouse femoral artery denudation with a guide wire, 5-MTP accelerated recovery of endothelium in the denuded area and reduced vascular leakage and intimal thickening. 5-MTP increased endothelial cell proliferation in the denuded arteries and rescued TNF-&#x3B1;-reduced endothelial cell proliferation and migration, likely via maintaining vascular endothelial growth factor receptor 2 activation. In contrast, 5-MTP preserved differentiated phenotype of medial vascular smooth muscle cells (VSMCs) and decreased VSMC proliferation and migration. Furthermore, 5-MTP maintained expression levels of critical transcription factors for VSMC marker gene expressions via attenuated activation of p38 MAPK and NF&#x3BA;B-p65. Our findings uncover a novel protective mechanism of 5-MTP in restenosis. In response to denudation injury, 5-MTP attenuates intimal hyperplasia via concerted but opposing actions on endothelial cells and VSMCs. Taken together, our results suggest that 5-MTP is a valuable therapeutic target for arterial injury-induced restenosis.
                ER  -

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

TRIM59 loss in M2 macrophages promotes melanoma migration and invasion by upregulating MMP-9 and Madcam1

Yuan Tian, Yantong Guo, Pei Zhu, Dongxu Zhang, Shanshan Liu, Mengyan Tang, Yuanxin Wang, Zheng Jin, Dong Li, Dongmei Yan, Guiying Li, Xun Zhu,

https://doi.org/10.18632/aging.102351 pp 8623—8641

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Tian Y, Guo Y, Zhu P, Zhang D, Liu S, Tang M, Wang Y, Jin Z, Li D, Yan D, Li G, Zhu X, . TRIM59 loss in M2 macrophages promotes melanoma migration and invasion by upregulating MMP-9 and Madcam1. . 11:8623-8641. https://doi.org/10.18632/aging.102351

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Tian, Yuan 
                AU  - Guo, Yantong 
                AU  - Zhu, Pei 
                AU  - Zhang, Dongxu 
                AU  - Liu, Shanshan 
                AU  - Tang, Mengyan 
                AU  - Wang, Yuanxin 
                AU  - Jin, Zheng 
                AU  - Li, Dong 
                AU  - Yan, Dongmei 
                AU  - Li, Guiying 
                AU  - Zhu, Xun 
                TI  - TRIM59 loss in M2 macrophages promotes melanoma migration and invasion by upregulating MMP-9 and Madcam1
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102351
                DO  - 10.18632/aging.102351
                SP  - 8623
                EP  - 8641
                PY  - 
                AB  - The culture supernatant from macrophages overexpressing TRIM59 has a cytotoxic effect on melanoma, but the mechanism remains unclear. To investigate whether deletion of TRIM59 in macrophages affects the metastatic potential of melanoma cells, we polarized control and TRIM59-deficient bone marrow-derived macrophages to the M2 phenotype and collected the respective conditioned media (CM). Exposure to CM from TRIM59-/--M2 cultures significantly promoted migration and invasion by B16-F0 and B16-F10 cells. Cytokine profiling indicated a ~15-fold increase in TNF-&#x3B1; production in CM from TRIM59-/--M2 cultures, and neutralizing TNF-&#x3B1; activity abrogated the referred stimulatory effects on cell motility. Transcriptome analysis revealed significant upregulation of MMP-9 and Madcam1 in melanoma cells exposed to TRIM59-/--M2 CM. Inhibitory experiments determined that these changes were also TNF-&#x3B1;-dependent and mediated by activation of ERK signaling. Independent knockdown of MMP9 and Madcam1 in B16-F10 cells impeded epithelial-mesenchymal transition and inhibited subcutaneous tumor growth and formation of metastatic lung nodules in vivo. These data suggest TRIM59 expression attenuates the tumor-promoting effect of tumor-associated macrophages, most of which resemble the M2 phenotype. Moreover, they highlight the relevance of TRIM59 in macrophages as a potential regulator of tumor metastasis and suggest TRIM59 could serve as a novel target for cancer immunotherapy.
                ER  -

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

Decreased levels of circulating trimethylamine N-oxide alleviate cognitive and pathological deterioration in transgenic mice: a potential therapeutic approach for Alzheimer’s disease

Qiang Gao, Yuan Wang, Xin Wang, Shuang Fu, Xin Zhang, Rui-Tao Wang, Xin Zhang,

https://doi.org/10.18632/aging.102352 pp 8642—8663

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gao Q, Wang Y, Wang X, Fu S, Zhang X, Wang R, Zhang X, . Decreased levels of circulating trimethylamine N-oxide alleviate cognitive and pathological deterioration in transgenic mice: a potential therapeutic approach for Alzheimer’s disease. . 11:8642-8663. https://doi.org/10.18632/aging.102352

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gao, Qiang 
                AU  - Wang, Yuan 
                AU  - Wang, Xin 
                AU  - Fu, Shuang 
                AU  - Zhang, Xin 
                AU  - Wang, Rui-Tao 
                AU  - Zhang, Xin 
                TI  - Decreased levels of circulating trimethylamine N-oxide alleviate cognitive and pathological deterioration in transgenic mice: a potential therapeutic approach for Alzheimer’s disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102352
                DO  - 10.18632/aging.102352
                SP  - 8642
                EP  - 8663
                PY  - 
                AB  - Trimethylamine-N-oxide (TMAO), a metabolite of gut microbiota, has been implicated in the pathogenesis of Alzheimer&#x2019;s disease (AD). However, the mechanisms by which TMAO influence cognitive and pathological processes in the AD have not been investigated. In this study, we found that the circulating TMAO levels displayed an age-related increase in both WT and APP/PS1 mice and association with AD-like behavioral and pathological profile. Reduced TMAO by 3,3-Dimethyl-1-butanol (DMB) treatment ameliorated the cognitive deterioration and long-term potentiation (LTP) in APP/PS1 mice. Moreover, DMB treatment also induced a decrease in the Amyloid-&#x3B2; (A&#x3B2;)1-42, &#x3B2;-secretase, and &#x3B2;-secretase-cleaved C-terminal fragment (&#x3B2;CTF) levels in the hippocampus. Finally, the effects obtained after treatment with DMB were accompanied by a reduction in circulating clusterin levels and hippocampal neuroinflammatory status in APP/PS1 mice. These findings demonstrate that elevated circulating TMAO during the aging process might deteriorate cognitive function and pathology in APP/PS1 mice.
                ER  -

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

Decreased RIPK1 expression in chondrocytes alleviates osteoarthritis via the TRIF/MyD88-RIPK1-TRAF2 negative feedback loop

Shuang Liang, Zheng-Gang Wang, Zhen-Zhen Zhang, Kun Chen, Zheng-Tao Lv, Yu-Ting Wang, Peng Cheng, Kai Sun, Qing Yang, An-Min Chen,

https://doi.org/10.18632/aging.102354 pp 8664—8680

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liang S, Wang Z, Zhang Z, Chen K, Lv Z, Wang Y, Cheng P, Sun K, Yang Q, Chen A, . Decreased RIPK1 expression in chondrocytes alleviates osteoarthritis via the TRIF/MyD88-RIPK1-TRAF2 negative feedback loop. . 11:8664-8680. https://doi.org/10.18632/aging.102354

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liang, Shuang 
                AU  - Wang, Zheng-Gang 
                AU  - Zhang, Zhen-Zhen 
                AU  - Chen, Kun 
                AU  - Lv, Zheng-Tao 
                AU  - Wang, Yu-Ting 
                AU  - Cheng, Peng 
                AU  - Sun, Kai 
                AU  - Yang, Qing 
                AU  - Chen, An-Min 
                TI  - Decreased RIPK1 expression in chondrocytes alleviates osteoarthritis via the TRIF/MyD88-RIPK1-TRAF2 negative feedback loop
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102354
                DO  - 10.18632/aging.102354
                SP  - 8664
                EP  - 8680
                PY  - 
                AB  - Osteoarthritis (OA) is the most common degenerative joint disease and involves the loss of articular cartilage integrity, formation of articular osteophytes, remodeling of subchondral bone, and synovitis. Knockdown of receptor interacting serine/threonine kinase (RIPK) 1 leads to anti-inflammatory and anti-apoptotic effects. However, the involvement of RIPK1 in the pathogenesis of OA is unclear. Here, we evaluated the effect of RIPK1 on chondrocytes and elaborated the underlying molecular mechanism. Knockdown of RIPK1 protected chondrocytes against inflammation and apoptosis induced by interleukin (IL)-1&#x3B2; in vitro and in vivo. RIPK1 was required for myeloid differentiation primary response 88 (MyD88)- and TIR-domain-containing adapter-inducing interferon b (TRIF)-mediated production of matrix metalloproteinases (MMPs) in OA. Moreover, overexpression of RIPK1 promoted the expression of tumor necrosis factor receptor-associated factor 2 (TRAF2), which blocked the expression and phosphorylation of RIPK1. Upregulation of TRAF2 decreased the expression of TRIF, MyD88, and MMPs in chondrocytes. Furthermore, knockdown of RIPK1 blocked activation of the nuclear factor-&#x3BA;B (NF-&#x3BA;B) and c-Jun N-terminal kinase (JNK) signaling pathways. In summary, knockdown of RIPK1 alleviated OA in a manner mediated by the TRIF/MyD88-RIPK1-TRAF2 negative feedback loop and activation of the NF-&#x3BA;B and JNK signaling pathways.
                ER  -

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

The prognostic value of YAP1 on clinical outcomes in human cancers

Ying Wu, Yanshen Hou, Peng Xu, Yujiao Deng, Kang Liu, Meng Wang, Tian Tian, Cong Dai, Na Li, Qian Hao, Dingli Song, Ling hui Zhou, Zhijun Dai,

https://doi.org/10.18632/aging.102358 pp 8681—8700

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wu Y, Hou Y, Xu P, Deng Y, Liu K, Wang M, Tian T, Dai C, Li N, Hao Q, Song D, Zhou Lh, Dai Z, . The prognostic value of YAP1 on clinical outcomes in human cancers. . 11:8681-8700. https://doi.org/10.18632/aging.102358

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wu, Ying 
                AU  - Hou, Yanshen 
                AU  - Xu, Peng 
                AU  - Deng, Yujiao 
                AU  - Liu, Kang 
                AU  - Wang, Meng 
                AU  - Tian, Tian 
                AU  - Dai, Cong 
                AU  - Li, Na 
                AU  - Hao, Qian 
                AU  - Song, Dingli 
                AU  - Zhou, Ling hui 
                AU  - Dai, Zhijun 
                TI  - The prognostic value of YAP1 on clinical outcomes in human cancers
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102358
                DO  - 10.18632/aging.102358
                SP  - 8681
                EP  - 8700
                PY  - 
                AB  - Background: As an important downstream factor in the Hippo pathway, yes-associated protein 1(YAP1) has been detected to be elevated in various cancers and demonstrated to play a role in tumor development. Therefore, we evaluated by a meta-analysis the prognostic value of YAP1 in cancer patients.Results: Sixty-eight studies with 8631 patients were identified. The results indicated that YAP1 overexpression predicted unfavorable patient prognosis in studies with overall survival (OS) (HR=1.76, 95%CI: 1.50-2.06, p&lt;0.001) and disease-free survival (DFS) (HR=1.39, 95%CI: 1.22-1.59, p&lt;0.001), as well as in studies with recurrence-free survival (RFS) (HR=2.38, 95%CI: 1.73-3.27, p&lt;0.001), and disease-specific survival (DSS) (HR=2.04, 95%CI: 1.55-2.70, p&lt;0.001). Meanwhile, YAP1 overexpression was also observed to be significantly associated with worse OS in GEPIA (HR=1.2, p&lt;0.001).Conclusions: Overexpression of YAP1 showed great association with poorer prognosis in patients with various cancers, particularly liver cancer. Therefore, YAP1 might be an important prognostic marker and a novel target of cancer therapy.Methods: We searched for potential publications in several online databases and retrieved relevant data. Overall and subgroup analyses were performed. Begg&#x2019;s and Egger&#x2019;s tests were used to assess publication bias. Online dataset GEPIA was used to generate the survival curves and verify the prognostic role of YAP1 in patients with tumors.
                ER  -

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

Time-to-event analyses of lower-limb venous thromboembolism in aged patients undergoing lumbar spine surgery: a retrospective study of 1620 patients

Liang Li, Zhaohui Li, Yachong Huo, Dalong Yang, Wenyuan Ding, Sidong Yang,

https://doi.org/10.18632/aging.102364 pp 8701—8709

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li L, Li Z, Huo Y, Yang D, Ding W, Yang S, . Time-to-event analyses of lower-limb venous thromboembolism in aged patients undergoing lumbar spine surgery: a retrospective study of 1620 patients. . 11:8701-8709. https://doi.org/10.18632/aging.102364

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Liang 
                AU  - Li, Zhaohui 
                AU  - Huo, Yachong 
                AU  - Yang, Dalong 
                AU  - Ding, Wenyuan 
                AU  - Yang, Sidong 
                TI  - Time-to-event analyses of lower-limb venous thromboembolism in aged patients undergoing lumbar spine surgery: a retrospective study of 1620 patients
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102364
                DO  - 10.18632/aging.102364
                SP  - 8701
                EP  - 8709
                PY  - 
                AB  - After spine surgery, venous thromboembolism (VTE) is not uncommon in aged patients. This study investigates time-to-event risk factors of postoperative VTE based on medical records of aged patients (age&#x2265;60 yr) between January 2013 and December 2018. All participants had undergone lower extremity ultrasonography pre- and postoperatively at the first, second, fourth, eighth, and twelfth weeks. Mann-Whitney U tests and chi-square tests were used for univariate analyses, and Cox regression was utilized for multivariate analyses. A total of 1620 cases were recruited, VTE group (N=382, 23.6%) and non-VTE group (N=1238, 76.4%), aged 67 (IQR 11) years and 65 (IQR 6) years, respectively. The univariate analyses indicated significant differences between the VTE and non-VTE groups regarding advanced age, VTE history, hypertension, fusion, hospital stay, FIB, HDL, D-dimer, and TC (all P&lt;0.05). The Cox regression showed that advanced age (OR=1.108; 95% CI, 1.091&#x2013;1.126), VTE history (OR=4.962; 95% CI, 3.849&#x2013;6.397), and hypertension (OR=1.344; 95% CI, 1.084&#x2013;1.667) were the risk factors for postoperative VTE (P&lt;0.05). The time-to-event analyses indicated that the hazard of VTE formation was highest in the first postoperative week. In conclusion, advanced age, VTE history, and hypertension are main risks for VTE formation, particularly in the first postoperative week.
                ER  -

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

Association of a novel seven-gene expression signature with the disease prognosis in colon cancer patients

Haojie Yang, Hua Liu, Hong-Cheng Lin, Dan Gan, Wei Jin, Can Cui, Yixin Yan, Yiming Qian, Changpeng Han, Zhenyi Wang,

https://doi.org/10.18632/aging.102365 pp 8710—8727

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Yang H, Liu H, Lin H, Gan D, Jin W, Cui C, Yan Y, Qian Y, Han C, Wang Z, . Association of a novel seven-gene expression signature with the disease prognosis in colon cancer patients. . 11:8710-8727. https://doi.org/10.18632/aging.102365

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Yang, Haojie 
                AU  - Liu, Hua 
                AU  - Lin, Hong-Cheng 
                AU  - Gan, Dan 
                AU  - Jin, Wei 
                AU  - Cui, Can 
                AU  - Yan, Yixin 
                AU  - Qian, Yiming 
                AU  - Han, Changpeng 
                AU  - Wang, Zhenyi 
                TI  - Association of a novel seven-gene expression signature with the disease prognosis in colon cancer patients
                JO  - 
                JA  - 
                VL  - 11
                IS  - 19
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102365
                DO  - 10.18632/aging.102365
                SP  - 8710
                EP  - 8727
                PY  - 
                AB  - Older patients who are diagnosed with colon cancer face unique challenges, specifically regarding to cancer treatment. The aim of this study was to identify prognostic signatures to predicting prognosis in colon cancer patients through a detailed transcriptomic analysis. RNA-seq expression profile, miRNA expression profile, and clinical phenotype information of all the samples of TCGA colon adenocarcinoma were downloaded and differentially expressed mRNAs (DEMs), differentially expressed lncRNAs (DELs) and differentially expressed miRNAs (DEMis) were identified. A competing endogenous RNA (ceRNA) network was constructed further and DEMs related with prognosis in the ceRNA network was screened using Cox regression analysis. Risk score models for predicting the prognosis of colon cancer patients were built using these DEMs. A total of 1476 DEMs, 9 DELs, and 243 DEMis between the tumor and normal samples were identified and functional enrichment analyses showed that the DEMs were significantly enriched in the nervous system development, ribosome biogenesis pathways in eukaryotes, and drug metabolism cytochrome P450. Twelve DEMs related with prognosis were screened from the ceRNA network. Thereafter, the risk score models of prognostic DEMs were obtained, involving seven DEMs (SGCG, CLDN23, SLC4A4, CCDC78, SLC17A7, OTOP3, and SMPDL3A). Additionally, cancer stage was identified as a prognostic clinical factor. This prognostic signature was further validated in two independent datasets. Our study developed a seven-mRNA and one-clinical factor signature that are associated with prognosis in colon cancer patients, which may serve as possible biomarkers and therapeutic targets in the future.
                ER  -

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

Correction for: Real-world effectiveness of medications on survival in patients with COPD-heart failure overlap

Vincent Yi-Fong Su, Yao-Hsu Yang, Diahn-Warng Perng, Ying-Huang Tsai, Kun-Ta Chou, Kang-Cheng Su, Wei-Juin Su, Pau-Chung Chen, Kuang-Yao Yang,

https://doi.org/10.18632/aging.102363 pp 8728—8729

PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Su VY, Yang Y, Perng D, Tsai Y, Chou K, Su K, Su W, Chen P, Yang K, . Correction for: Real-world effectiveness of medications on survival in patients with COPD-heart failure overlap. . 11:8728-8729. https://doi.org/10.18632/aging.102363

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

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

Volume 11, Issue 19

About the Cover

Editorials

Gianluca Civenni, Giuseppina M. Carbone, Carlo V. Catapano,

Cite this Article

How to cite

Copy or Download citation:

Nir Hacohen, Yuk Yuen Lan,

Cite this Article

How to cite

Copy or Download citation:

Torben Mentrup, Bernd Schröder,

Cite this Article

How to cite

Copy or Download citation:

Ravirajsinh N. Jadeja, Pamela M. Martin,

Cite this Article

How to cite

Copy or Download citation:

Jaewon Min, Jerry W. Shay,

Cite this Article

How to cite

Copy or Download citation:

Research Perspective

Mikhail V. Blagosklonny,

Cite this Article

How to cite

Copy or Download citation:

Research Papers

Yanping Hu, Yixun Zhao, Chao Shi, Pengfei Ren, Bing Wei, Yongjun Guo, Jie Ma,

Cite this Article

How to cite

Copy or Download citation:

Chun-Hsu Pan, Chang-Jui Chen, Chun-Ming Shih, Ming-Fu Wang, Jie-Yu Wang, Chieh-Hsi Wu,

Cite this Article

How to cite

Copy or Download citation:

Yewei Jia, Jiawei Jiang, Kangxian Zhao, Tan Zhang, Peng Sun, Jiaxuan Peng, Qichang Yang, Yu Qian,

Cite this Article

How to cite

Copy or Download citation:

Shuang Xu, Huaner Ni, Hangwei Chen, Qiuyan Dai,

Cite this Article

How to cite

Copy or Download citation:

Lei Ding, Yuan Tian, Ling Wang, Miaomiao Bi, Dengke Teng, Sen Hong,

Cite this Article

How to cite

Copy or Download citation:

Yaxin Hu, Liangzhao Chu, Jian Liu, Lei Yu, Shi-bin Song, Hua Yang, Feng Han,

Cite this Article

How to cite

Copy or Download citation:

Wen-Chao Li, Zhi-Yong Xiong, Pin-Zhu Huang, Yang-Jing Liao, Quan-Xi Li, Zhi-Cheng Yao, Ya-Di Liao, Shi-Lei Xu, Hui Zhou, Qing-Liang Wang, He Huang, Peng Zhang, Ji-Zong Lin, Bo Liu, Jie Ren, Kun-Peng Hu,

Cite this Article

How to cite

Copy or Download citation:

Yang Su, Xiurui Lv, Wei Yin, Lingling Zhou, Yilin Hu, Ang Zhou, FuZhen Qi,

Cite this Article

How to cite

Copy or Download citation:

Peng-Fei Zhang, Jing Wu, Jin-Hong Luo, Ke-Sang Li, Fei Wang, Wei Huang, Yin Wu, Shui-Ping Gao, Xue-Mei Zhang, Peng-Nan Zhang,

Cite this Article

How to cite

Copy or Download citation:

In-Suk Bae, Jae Min Kim, Jin Hwan Cheong, Je Il Ryu, Myung-Hoon Han,

Cite this Article

How to cite

Copy or Download citation:

Beilin Zhang, Shaokuan Fang, Yingying Cheng, Chunkui Zhou, Fang Deng,

Cite this Article

How to cite

Copy or Download citation:

Nguyen Chi Tai, Soo-A Kim, Sang-Gun Ahn,

Cite this Article

How to cite

Copy or Download citation:

Xiaoliang Huang, Jungang Liu, Xianwei Mo, Haizhou Liu, Chunyin Wei, Lingxu Huang, Jianhong Chen, Chao Tian, Yongsheng Meng, Guo Wu, Weishun Xie, Franco Jeen P.C., Zujun Liu, Weizhong Tang,

Cite this Article

How to cite