Volume 11, Issue 5

Guo X, Li L, Gao Z, Zhou H, Li J, Wang Q, . The long non-coding RNA PTTG3P promotes growth and metastasis of cervical cancer through PTTG1. . 11:1333-1341. https://doi.org/10.18632/aging.101830

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                TY  - JOUR
                AU  - Guo, Xiang-cui 
                AU  - Li, Li 
                AU  - Gao, Zhi-hui 
                AU  - Zhou, Hong-wei 
                AU  - Li, Jun 
                AU  - Wang, Qian-qing 
                TI  - The long non-coding RNA PTTG3P promotes growth and metastasis of cervical cancer through PTTG1
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101830
                DO  - 10.18632/aging.101830
                SP  - 1333
                EP  - 1341
                PY  - 
                AB  - The outgrowth and metastasis of cervical cancer (CC) contribute to its malignancy. Pituitary Tumor Transforming Gene 1 (PTTG1) is upregulated in many types of cancer, and enhances tumor cell growth and metastasis. However, the activation and regulation of PTTG1 in CC, especially by its pseudogene PTTG3P, have not been shown. Here, we detected significantly higher levels of PTTG1 and PTTG3P in the resected CC tissue, compared to the paired adjacent normal cervical tissue. Interestingly, the PTTG3P levels positively correlated with the PTTG1 levels. High PTTG3P levels were associated with poor patients’ survival. In vitro, PTTG1 were increased by PTTG3P overexpression, but was inhibited by PTTG3P depletion in CC cells. However, PTTG3P levels were not altered by modulation of PTTG1 in CC cells, suggesting that PTTG3P is upstream of PTTG1. Moreover, PTTG3P increased CC cell growth, likely through CCNB1-mediated increase in cell proliferation, rather than through decrease in cell apoptosis. Furthermore, PTTG3P increased CC cell invasiveness, likely through upregulation of SNAIL and downregulation of E-cadherin. Our work thus suggests that PTTG3P may promote growth and metastasis of CC through PTTG1.
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MicroRNA-127 inhibits cell proliferation via targeting Kif3b in pancreatic β cells

Ziyang Shen, Hemin Jiang, Hsiang-Ting Hsu, Li Qian, Qi Fu, Min Shen, Shu Chen, Tao Yang,

https://doi.org/10.18632/aging.101835 pp 1342—1355

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Shen Z, Jiang H, Hsu H, Qian L, Fu Q, Shen M, Chen S, Yang T, . MicroRNA-127 inhibits cell proliferation via targeting Kif3b in pancreatic β cells. . 11:1342-1355. https://doi.org/10.18632/aging.101835

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                TY  - JOUR
                AU  - Shen, Ziyang 
                AU  - Jiang, Hemin 
                AU  - Hsu, Hsiang-Ting 
                AU  - Qian, Li 
                AU  - Fu, Qi 
                AU  - Shen, Min 
                AU  - Chen, Shu 
                AU  - Yang, Tao 
                TI  - MicroRNA-127 inhibits cell proliferation via targeting Kif3b in pancreatic β cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101835
                DO  - 10.18632/aging.101835
                SP  - 1342
                EP  - 1355
                PY  - 
                AB  - MicroRNAs (miRNAs) have been implicated in β cells dysfunction. Previous studies indicated that miR-127 was specifically abundant in β cells and one of its target genes, Kif3b, promoted cell proliferation. However, the impact of the miR-127-Kif3b axis on β cells remains unknown. In this study, we revealed that miR-127 level was declined both in islets from the mice with a high-fat diet and in MIN6 cells with elevated glucose treatment. The elevated level of miR-127 attenuated β cell proliferation by repressing Kif3b expression without affecting apoptosis and cell cycle, and it dampened insulin secretion. Moreover, β cell-derived miR-127 could also affect the islet endothelial cell-line, MS1, in vitro via the transfer of extracellular vesicles (EVs). Treating MS1 cells with the EVs secreted by MIN6 cells exhibited a higher ability in cell migration and tube formation. However, this effect was abolished by the miR-127 inhibitor co-cultured with EVs-treated MS1 cells. Thus, we define that miR-127 is a crucial regulator of insulin secretion and cell proliferation in pancreatic β cells as well as a potential functional regulation factor in islet endothelial cells.
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Alternative polyadenylation dependent function of splicing factor SRSF3 contributes to cellular senescence

Ting Shen, Huan Li, Yifang Song, Li Li, Jinzhong Lin, Gang Wei, Ting Ni,

https://doi.org/10.18632/aging.101836 pp 1356—1388

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Shen T, Li H, Song Y, Li L, Lin J, Wei G, Ni T, . Alternative polyadenylation dependent function of splicing factor SRSF3 contributes to cellular senescence. . 11:1356-1388. https://doi.org/10.18632/aging.101836

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                TY  - JOUR
                AU  - Shen, Ting 
                AU  - Li, Huan 
                AU  - Song, Yifang 
                AU  - Li, Li 
                AU  - Lin, Jinzhong 
                AU  - Wei, Gang 
                AU  - Ni, Ting 
                TI  - Alternative polyadenylation dependent function of splicing factor SRSF3 contributes to cellular senescence
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101836
                DO  - 10.18632/aging.101836
                SP  - 1356
                EP  - 1388
                PY  - 
                AB  - Down-regulated splicing factor SRSF3 is known to promote cellular senescence, an important biological process in preventing cancer and contributing to individual aging, via its alternative splicing dependent function in human cells. Here we discovered alternative polyadenylation (APA) dependent function of SRSF3 as a novel mechanism explaining SRSF3 downregulation induced cellular senescence. Knockdown of SRSF3 resulted in preference usage of proximal poly(A) sites and thus global shortening of 3′ untranslated regions (3′ UTRs) of mRNAs. SRSF3-depletion also induced senescence-related phenotypes in both human and mouse cells. These 3′ UTR shortened genes were enriched in senescence-associated pathways. Shortened 3′ UTRs tended to produce more proteins than the longer ones. Simulating the effects of 3′ UTR shortening by overexpression of three candidate genes (PTEN, PIAS1 and DNMT3A) all led to senescence-associated phenotypes. Mechanistically, SRSF3 has higher binding density near proximal poly(A) site than distal one in 3′ UTR shortened genes. Further, upregulation of PTEN by either ectopic overexpression or SRSF3-knockdown induction both led to reduced phosphorylation of AKT and ultimately senescence-associated phenotypes. We revealed for the first time that reduced SRSF3 expression could promote cellular senescence through its APA-dependent function, largely extending our mechanistic understanding in splicing factor regulated cellular senescence.
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SP1-induced lncRNA TINCR overexpression contributes to colorectal cancer progression by sponging miR-7-5p

Shaojun Yu, Da Wang, Yingkuan Shao, Teng Zhang, Haiting Xie, Xiaomeng Jiang, Qun Deng, Yurong Jiao, Jinhua Yang, Cheng Cai, Lifeng Sun,

https://doi.org/10.18632/aging.101839 pp 1389—1403

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Yu S, Wang D, Shao Y, Zhang T, Xie H, Jiang X, Deng Q, Jiao Y, Yang J, Cai C, Sun L, . SP1-induced lncRNA TINCR overexpression contributes to colorectal cancer progression by sponging miR-7-5p. . 11:1389-1403. https://doi.org/10.18632/aging.101839

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                TY  - JOUR
                AU  - Yu, Shaojun 
                AU  - Wang, Da 
                AU  - Shao, Yingkuan 
                AU  - Zhang, Teng 
                AU  - Xie, Haiting 
                AU  - Jiang, Xiaomeng 
                AU  - Deng, Qun 
                AU  - Jiao, Yurong 
                AU  - Yang, Jinhua 
                AU  - Cai, Cheng 
                AU  - Sun, Lifeng 
                TI  - SP1-induced lncRNA TINCR overexpression contributes to colorectal cancer progression by sponging miR-7-5p
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101839
                DO  - 10.18632/aging.101839
                SP  - 1389
                EP  - 1403
                PY  - 
                AB  - Mounting evidences have indicated that long noncoding RNAs (lncRNAs) play pivotal roles in human diseases, especially in cancers. Recently, TINCR was proposed to be involved in tumor progression. However, its role in colorectal cancer (CRC) remains elusive. In our study, we found that SP1-induced TINCR was significantly upregulated in CRC tissues and cell lines. Moreover, cox multivariate survival analysis revealed that high TINCR was an independent predictor of poor overall survival (OS). Functionally, knockdown of TINCR obviously suppressed CRC cells proliferation, migration and invasion in vitro, and inhibited CRC cells growth and metastasis in vivo. Mechanistically, we identified TINCR could act as a miR-7-5p sponge using RNA pull down, luciferase reporter and RIP assays. Furthermore, we showed that TINCR might promote CRC progression via miR-7-5p-mediated PI3K/Akt/mTOR signaling pathway. Lastly, we revealed that plasma TINCR expression was upregulated in CRC when compared to healthy controls and could be a promising diagnostic biomarker for CRC. Based on above results, our data indicated that TINCR might serve as a potential diagnostic and prognostic biomarker for CRC.
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Age-dependent co-dependency structure of biomarkers in the general population of the United States

Alan Le Goallec, Chirag J. Patel,

https://doi.org/10.18632/aging.101842 pp 1404—1426

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Le Goallec A, Patel CJ, . Age-dependent co-dependency structure of biomarkers in the general population of the United States. . 11:1404-1426. https://doi.org/10.18632/aging.101842

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                TY  - JOUR
                AU  - Le Goallec, Alan 
                AU  - Patel, Chirag J. 
                TI  - Age-dependent co-dependency structure of biomarkers in the general population of the United States
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101842
                DO  - 10.18632/aging.101842
                SP  - 1404
                EP  - 1426
                PY  - 
                AB  - Phenotypic biomarkers (e.g. cholesterol, weight, and glucose) are important to diagnose and treat diseases associated with aging. However, while many biomarkers are co-dependent (e.g. glycohemoglobin and glucose), it is generally unknown how age influences their co-dependence. In the following, we analyzed 50 biomarkers in 27,508 National Health and Nutrition Examination Survey (NHANES) participants (age range: 20 to 80, mean age: 46.3 years old, sexes: 48.9% males, 51.1% females, ethnicities: 46.0% Whites, 27.8% Hispanics, 20.0% non-Hispanic Blacks, 6.1% others) to investigate how the co-dependency structure of common biomarkers evolves with age and whether differences exist between sexes and ethnicities. First, we associated the change in correlations between biomarkers with chronological age. We identified six trends and replicated our top finding (height vs. systolic blood pressure) in participants of the UK Biobank (N=470,895). We found that, on average, correlations tend to decrease with age. Secondly, we examined how biomarkers predict other biomarkers in participants of different age groups. We found 17 (34%) biomarkers whose predictability decreases with age and 5 (10%) biomarkers whose predictability increases with age. A limitation of this study is that it cannot distinguish between biological changes related to aging and generational effects. Our results can be interactively explored here: http://apps.chiragjpgroup.org/Aging_Biomarkers_Co-Dependencies/.
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FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway

Wei Ni, Yaoxiong Xia, Yuxu Bi, Fan Wen, Dong Hu, Lin Luo,

https://doi.org/10.18632/aging.101843 pp 1427—1439

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Ni W, Xia Y, Bi Y, Wen F, Hu D, Luo L, . FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway. . 11:1427-1439. https://doi.org/10.18632/aging.101843

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                TY  - JOUR
                AU  - Ni, Wei 
                AU  - Xia, Yaoxiong 
                AU  - Bi, Yuxu 
                AU  - Wen, Fan 
                AU  - Hu, Dong 
                AU  - Luo, Lin 
                TI  - FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101843
                DO  - 10.18632/aging.101843
                SP  - 1427
                EP  - 1439
                PY  - 
                AB  - Background/Aims: The present study was aimed at exploring the role of long noncoding RNA (lncRNA) FOXD2-AS1 in the development and progression of glioma and the underlying mechanism of FOXD2-AS1/miR-185-5p/HMGA2 network in glioma via regulation of PI3K/Akt signaling pathway.Methods: Microarray analysis was used for preliminary screening for candidate lncRNAs and mRNAs in glioma tissues. qRT-PCR and Western blot were used to determine the expression of FOXD2-AS1. The potential effects of FOXD2-AS1 on the viability, mobility and apoptosis of glioma cells were evaluated using MTT assay, Transwell assays and flow cytometry. The xenograft tumor model was performed to examine the influence of the lncRNA FOXD2-AS1/miR-185-5p/HMGA2 network on the biological functions of glioma cells. Luciferase assay and immunoprecipitation assay were examined to dissect molecular mechanisms.Results: LncRNA FOXD2-AS1 was overexpressed in human glioma, and upregulated FOXD2-AS11 expression indicated higher WHO grade (p &lt; 0.05). MiR-185-5p was downregulated, whereas HMGA2 was upregulated in glioma tissues in comparison with para-carcinoma tissues. FOXD2-AS1 could regulate the expression of HMGA2 via miR-185-5p. Knockdown of FOXD2-AS1 significantly inhibited proliferation and metastatic potential of glioma cells, whereas endogenous expression FOXD2-AS1 inhibited the glioma cell activity through targeting HMGA2.Conclusions: lncRNA FOXD2-AS1 acted as a sponge of miR-185-5p and influenced the PI3K/Akt signaling pathway through regulating HMGA2. LncRNA FOXD2-AS1 modulated HMGA2 and PI3K/Akt downstream signaling through sponging miR-185-5p, thereby promoting tumorigenesis and progression of glioma.
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Genetic variation underlying cognition and its relation with neurological outcomes and brain imaging

Maria J. Knol, Alis Heshmatollah, Lotte G.M. Cremers, M. Kamran Ikram, André G. Uitterlinden, Cornelia M. van Duijn, Wiro J. Niessen, Meike W. Vernooij, M. Arfan Ikram, Hieab H.H. Adams,

https://doi.org/10.18632/aging.101844 pp 1440—1456

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Knol MJ, Heshmatollah A, Cremers LG, Ikram MK, Uitterlinden AG, van Duijn CM, Niessen WJ, Vernooij MW, Ikram MA, Adams HH, . Genetic variation underlying cognition and its relation with neurological outcomes and brain imaging. . 11:1440-1456. https://doi.org/10.18632/aging.101844

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                TY  - JOUR
                AU  - Knol, Maria J. 
                AU  - Heshmatollah, Alis 
                AU  - Cremers, Lotte G.M. 
                AU  - Ikram, M. Kamran 
                AU  - Uitterlinden, André G. 
                AU  - van Duijn, Cornelia M. 
                AU  - Niessen, Wiro J. 
                AU  - Vernooij, Meike W. 
                AU  - Ikram, M. Arfan 
                AU  - Adams, Hieab H.H. 
                TI  - Genetic variation underlying cognition and its relation with neurological outcomes and brain imaging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101844
                DO  - 10.18632/aging.101844
                SP  - 1440
                EP  - 1456
                PY  - 
                AB  - Cognition in adults shows variation due to developmental and degenerative components. A recent genome-wide association study identified genetic variants for general cognitive function in 148 independent loci. Here, we aimed to elucidate possible developmental and neurodegenerative pathways underlying these genetic variants by relating them to functional, clinical and neuroimaging outcomes. This study was conducted within the population-based Rotterdam Study (N=11,496, mean age 65.3±9.9 years, 58.0% female). We used lead variants for general cognitive function to construct a polygenic score (PGS), and additionally excluded developmental variants at multiple significance thresholds. A higher PGS was related to more years of education (β=0.29, p=4.3x10-7) and a larger intracranial volume (β=0.05, p=7.5x10-4). To a smaller extent, the PGS was associated with less cognitive decline (βΔG-factor=0.03, p=1.3x10-3), which became non-significant after adjusting for education (p=1.6x10-2). No associations were found with daily functioning, dementia, parkinsonism, stroke or microstructural white matter integrity. Excluding developmental variants attenuated nearly all associations. In conclusion, this study suggests that the genetic variants identified for general cognitive function are acting mainly through the developmental pathway of cognition. Therefore, cognition, assessed cross-sectionally, seems to have limited value as a biomarker for neurodegeneration.
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Long intergenic non-coding LINC00657 regulates tumorigenesis of glioblastoma by acting as a molecular sponge of miR-190a-3p

Liangzhao Chu, Lei Yu, Jian Liu, Shibin Song, Hua Yang, Feng Han, Fen Liu, Yaxin Hu,

https://doi.org/10.18632/aging.101845 pp 1456—1470

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Chu L, Yu L, Liu J, Song S, Yang H, Han F, Liu F, Hu Y, . Long intergenic non-coding LINC00657 regulates tumorigenesis of glioblastoma by acting as a molecular sponge of miR-190a-3p. . 11:1456-1470. https://doi.org/10.18632/aging.101845

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                TY  - JOUR
                AU  - Chu, Liangzhao 
                AU  - Yu, Lei 
                AU  - Liu, Jian 
                AU  - Song, Shibin 
                AU  - Yang, Hua 
                AU  - Han, Feng 
                AU  - Liu, Fen 
                AU  - Hu, Yaxin 
                TI  - Long intergenic non-coding LINC00657 regulates tumorigenesis of glioblastoma by acting as a molecular sponge of miR-190a-3p
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101845
                DO  - 10.18632/aging.101845
                SP  - 1456
                EP  - 1470
                PY  - 
                AB  - To detect the aberrantly expressed long non-coding RNAs in glioblastoma, two pairs of glioblastoma and adjacent normal tissues were firstly analyzed by RNA sequencing. Long intergenic non-coding RNA LINC00657 was considered to play a vital role in glioblastoma based on the results of RNA sequencing. Hence, we aimed to investigate the mechanisms by which LINC00657 regulated the tumorigenesis of glioblastoma. The level of LINC00657 in 40 glioblastoma samples and glioblastoma cell lines was detected by RT-qPCR. LINC00657 was significantly decreased in patients with glioblastoma compared with adjacent normal tissues. Overexpression of LINC00657 inhibited proliferation, colony formation, invasion and migration in glioma cells via inducing apoptosis. Dual luciferase report assay indicated LINC00657 was the target of miR-190a-3p. Overexpression of LINC00657 greatly inhibited the relative amount of miR-190a-3p. Besides, miR-190a-3p was found to be a negative regulator of PTEN. Additionally, active-caspase 3 was increased in cells transfected with pcDNA3.1-LINC00657. Finally, in vitro results were further confirmed by in vivo studies using nude mice bearing with glioblastoma tumors. In conclusion, LINC00657 was effective in inhibiting glioblastoma by acting as a molecular sponge of miR-190a-3p to regulate PTEN expression. Therefore, targeting LINC00657 may serve as a potential strategy for the treatment of patients with glioblastoma.
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LINC00702 suppresses proliferation and invasion in non-small cell lung cancer through regulating miR-510/PTEN axis

Wencheng Yu, Daowei Li, Xiaoyan Ding, Yong Sun, Yanli Liu, Jinpeng Cong, Jiong Yang, Jian Sun, Xuchao Ning, Hongmei Wang, Tao Xu,

https://doi.org/10.18632/aging.101846 pp 1471—1485

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Yu W, Li D, Ding X, Sun Y, Liu Y, Cong J, Yang J, Sun J, Ning X, Wang H, Xu T, . LINC00702 suppresses proliferation and invasion in non-small cell lung cancer through regulating miR-510/PTEN axis. . 11:1471-1485. https://doi.org/10.18632/aging.101846

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                TY  - JOUR
                AU  - Yu, Wencheng 
                AU  - Li, Daowei 
                AU  - Ding, Xiaoyan 
                AU  - Sun, Yong 
                AU  - Liu, Yanli 
                AU  - Cong, Jinpeng 
                AU  - Yang, Jiong 
                AU  - Sun, Jian 
                AU  - Ning, Xuchao 
                AU  - Wang, Hongmei 
                AU  - Xu, Tao 
                TI  - LINC00702 suppresses proliferation and invasion in non-small cell lung cancer through regulating miR-510/PTEN axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101846
                DO  - 10.18632/aging.101846
                SP  - 1471
                EP  - 1485
                PY  - 
                AB  - Background: Long non-coding RNAs (lncRNAs) have been consistently reported to be involved in the progression of non-small cell lung cancer (NSCLC). In this study, we aimed to identify aberrantly expressed lncRNAs in NSCLC, in order to explore new therapeutic targets for NSCLC.Methods: Two pairs of NSCLC and adjacent normal tissues were first analyzed by RNA sequencing. The expressions of LINC00702 in 40 pairs patient samples and in 4 NSCLC cell lines was measured by quantitative real-time PCR. Putative target miRNAs of LINC00702 were predicted by the bioinformatics tools. The effect of LINC00702 on tumor growth in vivo was evaluated.Results: LINC00702 was significantly down-regulated in patients with NSCLC, which was correlated with tumor size and metastasis. In addition, overexpression of LINC00702 markedly suppressed proliferation and metastasis in NSCLC cells via inducing apoptosis in vitro and in vivo. Moreover, bioinformatics and luciferase reporter assays demonstrated that LINC00702 functioned as a competing endogenous RNA (ceRNA) for miR-510 in NSCLC, and upregulated its target gene PTEN.Conclusion: Our results indicated that LINC00702 modulated the expression of PTEN gene by acting as a ceRNA for miR-510 in NSCLC. Therefore, LINC00702 may serve as a potential target for the diagnosis and treatment of patients with NSCLC.
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Integrated DNA methylation and gene expression analysis in the pathogenesis of coronary artery disease

Liu Miao, Rui-Xing Yin, Qing-Hui Zhang, Xi-Jiang Hu, Feng Huang, Wu-Xian Chen, Xiao-Li Cao, Jin-Zhen Wu,

https://doi.org/10.18632/aging.101847 pp 1486—1500

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Miao L, Yin R, Zhang Q, Hu X, Huang F, Chen W, Cao X, Wu J, . Integrated DNA methylation and gene expression analysis in the pathogenesis of coronary artery disease. . 11:1486-1500. https://doi.org/10.18632/aging.101847

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                TY  - JOUR
                AU  - Miao, Liu 
                AU  - Yin, Rui-Xing 
                AU  - Zhang, Qing-Hui 
                AU  - Hu, Xi-Jiang 
                AU  - Huang, Feng 
                AU  - Chen, Wu-Xian 
                AU  - Cao, Xiao-Li 
                AU  - Wu, Jin-Zhen 
                TI  - Integrated DNA methylation and gene expression analysis in the pathogenesis of coronary artery disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101847
                DO  - 10.18632/aging.101847
                SP  - 1486
                EP  - 1500
                PY  - 
                AB  - To evaluate DNA methylation sites and gene expression associated with coronary artery disease (CAD) and the possible pathological mechanism involved, we performed (1) genome-wide DNA methylation and mRNA expression profiling in peripheral blood datasets from the Gene Expression Omnibus repository of CAD samples and controls; (2) functional enrichment analysis and differential methylation gene regulatory network construction; (3) validation tests of 11 differential methylation positions of interest and the corresponding gene expression; and (4) correlation analysis for DNA methylation and mRNA expression data. A total of 669 differentially expressed mRNAs were matched to differentially methylated genes. After disease ontology, Kyoto Encyclopedia of Genes and Genomes pathway, gene ontology, protein-protein interaction and network construction and module analyses, 11 differentially methylated positions (DMPs) corresponding to 11 unique genes were observed: BDNF – cg26949694, BTRC - cg24381155, CDH5 - cg02223351, CXCL12 - cg11267527, EGFR - cg27637738, IL-6 - cg13104385, ITGB1 - cg20545410, PDGFRB - cg25613180, PIK3R1- cg00559992, PLCB1 - cg27178677 and PTPRC - cg09247619. After validation tests of 11 DMPs of interest and the corresponding gene expression, we found that CXCL12 was less hypomethylated in the CAD group, whereas the relative expression of ITGB1, PDGFRB and PIK3R1 was lower in CAD samples, and CXCL12 and ITGB1 methylation was negatively correlated with their expression. This study identified the correlation between DNA methylation and gene expression and highlighted the importance of CXCL12 in CAD pathogenesis.
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Curcumin inhibits liver metastasis of gastric cancer through reducing circulating tumor cells

Xixi Gu, Qiqi Zhang, Wei Zhang, Liang Zhu,

https://doi.org/10.18632/aging.101848 pp 1501—1509

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Gu X, Zhang Q, Zhang W, Zhu L, . Curcumin inhibits liver metastasis of gastric cancer through reducing circulating tumor cells. . 11:1501-1509. https://doi.org/10.18632/aging.101848

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                TY  - JOUR
                AU  - Gu, Xixi 
                AU  - Zhang, Qiqi 
                AU  - Zhang, Wei 
                AU  - Zhu, Liang 
                TI  - Curcumin inhibits liver metastasis of gastric cancer through reducing circulating tumor cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101848
                DO  - 10.18632/aging.101848
                SP  - 1501
                EP  - 1509
                PY  - 
                AB  - Primary gastric cancer (PGC) is the fourth most common malignant human cancer and the second leading cause of death worldwide. The majority of the subjects of PGC is diagnosed at a late stage, resulting in poor prognosis and therapeutic outcome, largely attributable to dissemination of tumor cells into circulation as circulating tumor cells (CTCs) and their formation of distal tumor. Curcumin is an active ingredient from the rhizome of the plant Curcuma longa. Here, we assessed whether treatment with Curcumin may reduce the incidence of metastatic tumor formation in liver in mice carrying PGC. We found that Curcumin treatment significantly reduced the presence of CTCs and formation of liver tumor. Mechanistically, Curcumin reduced CXCR4 expression in PGCs in vitro and in vivo, and thus likely inhibited metastasis of PGC through suppression of stromal cell -derived factor-1/CXCR4 signaling. Thus, our study suggests that Curcumin may inhibit liver metastasis of PGC through reducing CTCs.
                ER  -

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Delayed γH2AX foci disappearance in mammary epithelial cells from aged women reveals an age-associated DNA repair defect

Teresa Anglada, Joan Repullés, Anna Espinal, Mark A LaBarge, Martha R Stampfer, Anna Genescà, Marta Martín,

https://doi.org/10.18632/aging.101849 pp 1510—1523

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Anglada T, Repullés J, Espinal A, LaBarge MA, Stampfer MR, Genescà A, Martín M, . Delayed γH2AX foci disappearance in mammary epithelial cells from aged women reveals an age-associated DNA repair defect. . 11:1510-1523. https://doi.org/10.18632/aging.101849

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Provider: 
                TY  - JOUR
                AU  - Anglada, Teresa 
                AU  - Repullés, Joan 
                AU  - Espinal, Anna 
                AU  - LaBarge, Mark A 
                AU  - Stampfer, Martha R 
                AU  - Genescà, Anna 
                AU  - Martín, Marta 
                TI  - Delayed γH2AX foci disappearance in mammary epithelial cells from aged women reveals an age-associated DNA repair defect
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101849
                DO  - 10.18632/aging.101849
                SP  - 1510
                EP  - 1523
                PY  - 
                AB  - Aging is a degenerative process in which genome instability plays a crucial role. To gain insight into the link between organismal aging and DNA repair capacity, we analyzed DNA double-strand break (DSB) resolution efficiency in human mammary epithelial cells from 12 healthy donors of young and old ages. The frequency of DSBs was measured by quantifying the number of γH2AX foci before and after 1Gy of γ-rays and it was higher in cells from aged donors (ADs) at all times analyzed. At 24 hours after irradiation, ADs retained a significantly higher frequency of residual DSBs than young donors (YDs), which had already reached values close to basal levels. The kinetics of DSB induction and disappearance showed that cells from ADs and YDs repair DSBs with similar speed, although analysis of early times after irradiation indicate that a repair defect may lie within the firing of the DNA repair machinery in AD cells. Indeed, using a mathematical model we calculated a constant factor of delay affecting aged human epithelial cells repair kinetics. This defect manifests with the accumulation of DSBs that might eventually undergo illegitimate repair, thus posing a relevant threat to the maintenance of genome integrity in older individuals.
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Influence of metabolic syndrome on the relationship between fatty acids and the selected parameters in men with benign prostatic hyperplasia

Katarzyna Grzesiak, Aleksandra Rył, Weronika Ratajczak, Ewa Stachowska, Iwona Rotter, Marcin Słojewski, Olimpia Sipak, Kinga Walczakiewicz, Maria Laszczyńska,

https://doi.org/10.18632/aging.101850 pp 1524—1536

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Grzesiak K, Rył A, Ratajczak W, Stachowska E, Rotter I, Słojewski M, Sipak O, Walczakiewicz K, Laszczyńska M, . Influence of metabolic syndrome on the relationship between fatty acids and the selected parameters in men with benign prostatic hyperplasia. . 11:1524-1536. https://doi.org/10.18632/aging.101850

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                TY  - JOUR
                AU  - Grzesiak, Katarzyna 
                AU  - Rył, Aleksandra 
                AU  - Ratajczak, Weronika 
                AU  - Stachowska, Ewa 
                AU  - Rotter, Iwona 
                AU  - Słojewski, Marcin 
                AU  - Sipak, Olimpia 
                AU  - Walczakiewicz, Kinga 
                AU  - Laszczyńska, Maria 
                TI  - Influence of metabolic syndrome on the relationship between fatty acids and the selected parameters in men with benign prostatic hyperplasia
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101850
                DO  - 10.18632/aging.101850
                SP  - 1524
                EP  - 1536
                PY  - 
                AB  - The purpose of our investigation was to analyze the relationship between the serum levels of fatty acids and their metabolites and the levels of the selected metabolic and hormonal parameters in patients with benign prostatic hyperplasia (BPH) with regard to concomitant metabolic syndrome (MetS). We determined serum concentrations of total (TT) and free testosterone (FT), insulin (I), dehydroepiandrosterone sulphate (DHEAS), luteinizing hormone and insulin-like growth factor 1 (IGF-1) and sex hormone-binding globulin (SHBG). Gas chromatography was performed. The patients differed in terms of hormone levels, but only the differences in SHBG and IGF-1 levels were statistically significant. Analysis of the levels of polysaturated fatty acids in BPH patients showed that MetS contributed to changes in the levels of these acids. We also analyzed the relationship between the levels of fatty acids and diagnostic parameters for MetS. Particular abnormalities were associated with single changes in the levels of fatty acids. In the diabetic patients, changes in the levels of pentadecanoic acid, heptadecanoic acid and cis-11-eicosenoic acid were demonstrated. Our findings indicate the necessity for further investigation concerning the levels of fatty acids and their impact on the development of MetS, as well as the course and clinical picture of BPH.
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Hepatic resection for hepatocellular carcinoma in the octogenarian: is it justified?

Chao-Wei Lee, Kun-Ming Chan, Hsin-I Tsai, Yi-Chung Hsieh, Cheng-Yu Lin, Yung-Chia Kuo, Heng-Yuan Hsu, Ming-Chin Yu,

https://doi.org/10.18632/aging.101854 pp 1537—1550

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Lee C, Chan K, Tsai H, Hsieh Y, Lin C, Kuo Y, Hsu H, Yu M, . Hepatic resection for hepatocellular carcinoma in the octogenarian: is it justified?. . 11:1537-1550. https://doi.org/10.18632/aging.101854

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                TY  - JOUR
                AU  - Lee, Chao-Wei 
                AU  - Chan, Kun-Ming 
                AU  - Tsai, Hsin-I 
                AU  - Hsieh, Yi-Chung 
                AU  - Lin, Cheng-Yu 
                AU  - Kuo, Yung-Chia 
                AU  - Hsu, Heng-Yuan 
                AU  - Yu, Ming-Chin 
                TI  - Hepatic resection for hepatocellular carcinoma in the octogenarian: is it justified?
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101854
                DO  - 10.18632/aging.101854
                SP  - 1537
                EP  - 1550
                PY  - 
                AB  - Liver resection is a standard treatment for hepatocellular carcinoma (HCC). The purpose of this study was to investigate the clinicopathological characteristics and long-term outcomes of octogenarians with HCC treated with liver resection. Records of patients who underwent liver resection for HCC were reviewed, and patients older and younger than 80 years were compared. There were 77 patients 80 years of age or older and 3,309 younger than 80 years. Hepatitis C virus infection was the most common etiology among the octogenarians (43.1%), followed by non-viral causes (37.5%). The older group had more co-morbidity but less hepatitis B virus infection and cirrhosis. More than 70% of the non-viral older group had diabetes mellitus, as compared to only 21.6% in the viral older group. The older group had rates of perioperative morbidity, mortality, disease-free survival, and overall survival comparable to the younger group (all p&gt;0.1). Multivariate analysis revealed that α-fetoprotein ≥400 ng/mL, tumor size ≥10 cm, and vascular invasion were independent prognostic factors for overall survival in the older patients. These findings demonstrate that liver resection is a justified treatment for HCC in octogenarians, and it can achieve surgical outcomes comparable to those in younger populations.
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Association of KRAS and NRAS gene polymorphisms with Wilms tumor risk: a four-center case-control study

Wen Fu, Zhenjian Zhuo, Rui-Xi Hua, Kai Fu, Wei Jia, Jinhong Zhu, Jiao Zhang, Jiwen Cheng, Haixia Zhou, Huimin Xia, Jing He, Guochang Liu,

https://doi.org/10.18632/aging.101855 pp 1551—1563

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Fu W, Zhuo Z, Hua R, Fu K, Jia W, Zhu J, Zhang J, Cheng J, Zhou H, Xia H, He J, Liu G, . Association of KRAS and NRAS gene polymorphisms with Wilms tumor risk: a four-center case-control study. . 11:1551-1563. https://doi.org/10.18632/aging.101855

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                TY  - JOUR
                AU  - Fu, Wen 
                AU  - Zhuo, Zhenjian 
                AU  - Hua, Rui-Xi 
                AU  - Fu, Kai 
                AU  - Jia, Wei 
                AU  - Zhu, Jinhong 
                AU  - Zhang, Jiao 
                AU  - Cheng, Jiwen 
                AU  - Zhou, Haixia 
                AU  - Xia, Huimin 
                AU  - He, Jing 
                AU  - Liu, Guochang 
                TI  - Association of <i>KRAS</i> and <i>NRAS</i> gene polymorphisms with Wilms tumor risk: a four-center case-control study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101855
                DO  - 10.18632/aging.101855
                SP  - 1551
                EP  - 1563
                PY  - 
                AB  - Wilms tumor is a type of pediatric solid tumor that arises partly due to somatic and germline mutations. Single-nucleotide polymorphisms (SNPs) in the RAS gene reportedly modify the risk for several types of human malignancies. We conducted a multicenter study to investigate whether RAS gene variants predispose individuals to Wilms tumor. Four SNPs in RAS were genotyped in 355 Wilms tumor cases and 1070 controls. The SNPs included rs12587 G&gt;T, rs7973450 A&gt;G and rs7312175 G&gt;A in KRAS, and rs2273267 A&gt;T in NRAS. Individuals harboring the rs12587 GT genotype were more likely to develop Wilms tumor than those carrying the GG genotype (adjusted odds ratio [OR]=1.30, 95% confidence interval [CI]=1.004-1.68, P=0.046). However, the other three SNPs seemed not to influence the risk for Wilms tumor. Compared to individuals without a risk genotype, those harboring one to three KRAS risk genotypes had an adjusted OR of 1.28 for developing Wilms tumor (95% CI=1.002-1.64, P=0.048). Stratification analysis revealed that rs12587 GT/TT was associated with Wilms tumor risk in children &gt;18 months old (adjusted OR=1.39, 95% CI=1.02-1.89, P=0.037). Our findings indicate that the rs12587 G&gt;T polymorphism in KRAS is associated with increased Wilms tumor susceptibility.
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Running wheel access fails to resolve impaired sustainable health in mice feeding a high fat sucrose diet

Aaffien C. Reijne, A. Talarovicova, Jolita Ciapaite, J.E. Bruggink, A. Bleeker, Albert K. Groen, Dirk-Jan Reijngoud, Barbara M. Bakker, Gertjan van Dijk,

https://doi.org/10.18632/aging.101857 pp 1564—1579

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Reijne AC, Talarovicova A, Ciapaite J, Bruggink J, Bleeker A, Groen AK, Reijngoud D, Bakker BM, van Dijk G, . Running wheel access fails to resolve impaired sustainable health in mice feeding a high fat sucrose diet. . 11:1564-1579. https://doi.org/10.18632/aging.101857

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                TY  - JOUR
                AU  - Reijne, Aaffien C. 
                AU  - Talarovicova, A. 
                AU  - Ciapaite, Jolita 
                AU  - Bruggink, J.E. 
                AU  - Bleeker, A. 
                AU  - Groen, Albert K. 
                AU  - Reijngoud, Dirk-Jan 
                AU  - Bakker, Barbara M. 
                AU  - van Dijk, Gertjan 
                TI  - Running wheel access fails to resolve impaired sustainable health in mice feeding a high fat sucrose diet
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101857
                DO  - 10.18632/aging.101857
                SP  - 1564
                EP  - 1579
                PY  - 
                AB  - Diet and physical activity are thought to affect sustainable metabolic health and survival. To improve understanding, we studied survival of mice feeding a low-fat (LF) or high-saturated fat/high sugar (HFS) diet, each with or without free running wheel (RW) access. Additionally several endocrine and metabolic health indices were assessed at 6, 12, 18 and 24 months of age. As expected, HFS feeding left-shifted survival curve of mice compared to LF feeding, and this was associated with increased energy intake and increased (visceral/total) adiposity, liver triglycerides, and increased plasma cholesterol, corticosterone, HOMA-IR, and lowered adiponectin levels. Several of these health parameters improved (transiently) by RW access in HFS and LF fed mice (i.e., HOMA-IR, plasma corticosterone), others however deteriorated (transiently) by RW access only in HFS-fed mice (i.e., body adiposity, plasma resistin, and free cholesterol levels). Apart from these multiple and sometimes diverging health effects of RW access, RW access did not affect survival curves. Important to note, voluntary RW activity declined with age, but this effect was most pronounced in the HFS fed mice. These results thus challenge the hypothesis that voluntary wheel running can counteract HFS-induced deterioration of survival and metabolic health.
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Influence of rapid eye movement sleep on all-cause mortality: a community-based cohort study

Jingjing Zhang, Xuting Jin, Ruohan Li, Ya Gao, Jiamei Li, Gang Wang,

https://doi.org/10.18632/aging.101858 pp 1580—1588

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Zhang J, Jin X, Li R, Gao Y, Li J, Wang G, . Influence of rapid eye movement sleep on all-cause mortality: a community-based cohort study. . 11:1580-1588. https://doi.org/10.18632/aging.101858

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                TY  - JOUR
                AU  - Zhang, Jingjing 
                AU  - Jin, Xuting 
                AU  - Li, Ruohan 
                AU  - Gao, Ya 
                AU  - Li, Jiamei 
                AU  - Wang, Gang 
                TI  - Influence of rapid eye movement sleep on all-cause mortality: a community-based cohort study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101858
                DO  - 10.18632/aging.101858
                SP  - 1580
                EP  - 1588
                PY  - 
                AB  - Introduction: Although the proportion and duration of rapid eye movement (REM) sleep are correlated with neurological and cardiovascular diseases, whether REM sleep is associated with all-cause mortality in community-based populations remains unknown.Methods: A prospective study was performed within the Sleep Heart Health Study (SHHS, Registration NO. NCT00005275). Total sleep time, sleep efficiency, and REM sleep were measured using polysomnography. Cox proportional hazards regression models were used to estimate the association of the REM sleep with all-cause mortality.Results: Over a mean follow-up period of 11.0 ± 3.1 y, 1234 individuals (21.9%) died. In the entire population, reduced REM sleep was significantly associated with increasing all-cause mortality. After adjustment for age, sex, race, body mass index, smoking status, total cholesterol, triglycerides, high-density lipoprotein, history of diabetes and hypertension, and the apnea–hypopnea index, the duration and proportion of REM sleep were found to be significantly associated with all-cause mortality when the lowest and the highest REM quartile groups were compared (hazard ratio, 95% confidence interval: 1.727, 1.434-2.079; 1.545, 1.298-1.839; respectively).Conclusion: The proportion and duration of REM sleep are negatively associated with all-cause mortality. This finding emphasizes the importance of personalized sleep management in community-based populations.
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Low triglyceride to high-density lipoprotein cholesterol ratio predicts hemorrhagic transformation in large atherosclerotic infarction of acute ischemic stroke

Qi-Wen Deng, Yu-Kai Liu, Yu-Qiao Zhang, Xiang-Liang Chen, Teng Jiang, Jian-Kang Hou, Hong-Chao Shi, Min Lu, Feng Zhou, Wei Wang, Shuo Li, Hui-Ling Sun, Jun-Shan Zhou,

https://doi.org/10.18632/aging.101859 pp 1589—1601

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Deng Q, Liu Y, Zhang Y, Chen X, Jiang T, Hou J, Shi H, Lu M, Zhou F, Wang W, Li S, Sun H, Zhou J, . Low triglyceride to high-density lipoprotein cholesterol ratio predicts hemorrhagic transformation in large atherosclerotic infarction of acute ischemic stroke. . 11:1589-1601. https://doi.org/10.18632/aging.101859

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                TY  - JOUR
                AU  - Deng, Qi-Wen 
                AU  - Liu, Yu-Kai 
                AU  - Zhang, Yu-Qiao 
                AU  - Chen, Xiang-Liang 
                AU  - Jiang, Teng 
                AU  - Hou, Jian-Kang 
                AU  - Shi, Hong-Chao 
                AU  - Lu, Min 
                AU  - Zhou, Feng 
                AU  - Wang, Wei 
                AU  - Li, Shuo 
                AU  - Sun, Hui-Ling 
                AU  - Zhou, Jun-Shan 
                TI  - Low triglyceride to high-density lipoprotein cholesterol ratio predicts hemorrhagic transformation in large atherosclerotic infarction of acute ischemic stroke
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101859
                DO  - 10.18632/aging.101859
                SP  - 1589
                EP  - 1601
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Deng, Qi-Wen 
                AU  - Liu, Yu-Kai 
                AU  - Zhang, Yu-Qiao 
                AU  - Chen, Xiang-Liang 
                AU  - Jiang, Teng 
                AU  - Hou, Jian-Kang 
                AU  - Shi, Hong-Chao 
                AU  - Lu, Min 
                AU  - Zhou, Feng 
                AU  - Wang, Wei 
                AU  - Li, Shuo 
                AU  - Sun, Hui-Ling 
                AU  - Zhou, Jun-Shan 
                TI  - Low triglyceride to high-density lipoprotein cholesterol ratio predicts hemorrhagic transformation in large atherosclerotic infarction of acute ischemic stroke
                JO  - 
                JA  - 
                VL  - 11
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101859
                DO  - 10.18632/aging.101859
                SP  - 1589
                EP  - 1601
                PY  - 
                AB  - The ratio of triglyceride (TG) to high-density lipoprotein cholesterol (HDL-C) is an objective approach to predicting poor outcomes in acute ischemic stroke (AIS). The impact of TG/HDL-C on hemorrhagic transformation (HT) after AIS remains unknown. The aim of this study was to explore the accurate effect of TG/HDL-C on HT after AIS. We enrolled a total of 1423 patients with AIS in the training cohort from a prospective, consecutive hospital-based stroke registry. Of the 1423 patients, HT occurred in 155 (10.89%) patients. The incidence of HT after AIS was significantly increased when there were low levels of TG (P=0.016) and TG/HDL-C (P=0.006) in patients with AIS attributable to large artery atherosclerosis (LAA), but not in those who suffered from cardioembolic stroke. After adjustment for covariates, a lower TG/HDL-C (OR=0.53, 95%CI=0.20-0.93) that was more than TG alone (OR=0.61, 95%CI=0.27-0.98) independently increased the risk of HT in LAA. Furthermore, our established nomogram indicated that lower TG/HDL-C was an indicator of HT. These findings were further validated in the test cohort of 558 patients with AIS attributable to LAA. In summary, a low level of TG/HDL-C is correlated with greater risk of HT after AIS attributable to LAA.
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Volume 11, Issue 5

About the Cover

Editorials

Christine M. Dengler-Crish, Florent Elefteriou,

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Diego Herrero, Antonio Bernad,

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Pierre-Alexandre Laurent, Bernard Payrastre, Marie-Pierre Gratacap,

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Carla S. B. Viegas, Dina C. Simes,

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Marco Bozzali, Marcello D’Amelio, Laura Serra,

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Moshi Song, Juan Carlos Izpisua Belmonte, Guang-Hui Liu,

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Kensuke Toyama, Masaki Mogi, Philip S. Tsao,

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Candice E. Van Skike, Veronica Galvan,

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Research Papers

Xiang-cui Guo, Li Li, Zhi-hui Gao, Hong-wei Zhou, Jun Li, Qian-qing Wang,

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Ziyang Shen, Hemin Jiang, Hsiang-Ting Hsu, Li Qian, Qi Fu, Min Shen, Shu Chen, Tao Yang,

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Ting Shen, Huan Li, Yifang Song, Li Li, Jinzhong Lin, Gang Wei, Ting Ni,

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Shaojun Yu, Da Wang, Yingkuan Shao, Teng Zhang, Haiting Xie, Xiaomeng Jiang, Qun Deng, Yurong Jiao, Jinhua Yang, Cheng Cai, Lifeng Sun,

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Alan Le Goallec, Chirag J. Patel,

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Wei Ni, Yaoxiong Xia, Yuxu Bi, Fan Wen, Dong Hu, Lin Luo,

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Maria J. Knol, Alis Heshmatollah, Lotte G.M. Cremers, M. Kamran Ikram, André G. Uitterlinden, Cornelia M. van Duijn, Wiro J. Niessen, Meike W. Vernooij, M. Arfan Ikram, Hieab H.H. Adams,

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Liangzhao Chu, Lei Yu, Jian Liu, Shibin Song, Hua Yang, Feng Han, Fen Liu, Yaxin Hu,

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Wencheng Yu, Daowei Li, Xiaoyan Ding, Yong Sun, Yanli Liu, Jinpeng Cong, Jiong Yang, Jian Sun, Xuchao Ning, Hongmei Wang, Tao Xu,

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Liu Miao, Rui-Xing Yin, Qing-Hui Zhang, Xi-Jiang Hu, Feng Huang, Wu-Xian Chen, Xiao-Li Cao, Jin-Zhen Wu,

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Xixi Gu, Qiqi Zhang, Wei Zhang, Liang Zhu,

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