Volume 11, Issue 23

Chen H, Lin W, Lin P, Zheng M, Lai Y, Chen M, Zhang Y, Chen J, Lin X, Lin L, Lan Q, Yuan Q, Chen R, et al, . IL-10 produces a dual effect on OGD-induced neuronal apoptosis of cultured cortical neurons via the NF-κB pathway. . 11:10796-10813. https://doi.org/10.18632/aging.102411

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                TY  - JOUR
                AU  - Chen, Hongbin 
                AU  - Lin, Wei 
                AU  - Lin, Peiqiang 
                AU  - Zheng, Mouwei 
                AU  - Lai, Yongxing 
                AU  - Chen, Manli 
                AU  - Zhang, Yixian 
                AU  - Chen, Jianhao 
                AU  - Lin, Xiaohui 
                AU  - Lin, Longzai 
                AU  - Lan, Quan 
                AU  - Yuan, Qilin 
                AU  - Chen, Ronghua 
                AU  - Jiang, Xinhong 
                AU  - Xiao, Yingchun 
                AU  - Liu, Nan 
                TI  - IL-10 produces a dual effect on OGD-induced neuronal apoptosis of cultured cortical neurons via the NF-κB pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102411
                DO  - 10.18632/aging.102411
                SP  - 10796
                EP  - 10813
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Chen, Hongbin 
                AU  - Lin, Wei 
                AU  - Lin, Peiqiang 
                AU  - Zheng, Mouwei 
                AU  - Lai, Yongxing 
                AU  - Chen, Manli 
                AU  - Zhang, Yixian 
                AU  - Chen, Jianhao 
                AU  - Lin, Xiaohui 
                AU  - Lin, Longzai 
                AU  - Lan, Quan 
                AU  - Yuan, Qilin 
                AU  - Chen, Ronghua 
                AU  - Jiang, Xinhong 
                AU  - Xiao, Yingchun 
                AU  - Liu, Nan 
                TI  - IL-10 produces a dual effect on OGD-induced neuronal apoptosis of cultured cortical neurons via the NF-κB pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102411
                DO  - 10.18632/aging.102411
                SP  - 10796
                EP  - 10813
                PY  - 
                AB  - As a classic immunoregulatory cytokine, interleukin-10 (IL-10) can provide in vivo and in vitro neuroprotection respectively during cerebral ischemia and after the oxygen-glucose deprivation (OGD)-induced injury. However, its role in cortical neuronal survival at different post-ischemic phases remains unclear. The current study found that IL-10 had distinct effects on the neuronal apoptosis at different OGD stages: at an early stage after OGD, IL-10 promoted the OGD-induced neuronal apoptosis in the cultured primary cortical neurons by activating p65 subunit, which up-regulated Bax expression and down-regulated Bcl-xL expression; at a late OGD stage, however, it attenuated the OGD-induced neuronal apoptosis by activating c-Rel, which up-regulated Bcl-xL expression and down-regulated Bax expression. The early-stage pro-apoptosis and late-stage anti-apoptosis were both partly abolished by PDTC, an NF-&#x3BA;B inhibitor, and promoted by PMA, an NF-&#x3BA;B activator. The optimal anti-apoptotic effect appeared when the cultured neurons were treated with IL-10 at 9-24 h after OGD. Taken together, our findings suggest that IL-10 exerts a dual effect on the survival of the cultured neurons by activating the NF-&#x3BA;B pathway at different stages after OGD injury and that PMA treatment at a late stage can facilitate the IL-10-conferred neuroprotection against OGD-induced neuronal injury.
                ER  -

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Long noncoding RNA LINC00958 accelerates the proliferation and matrix degradation of the nucleus pulposus by regulating miR-203/SMAD3

Kunchi Zhao, Yang Zhang, Hongping Yuan, Mingming Zhao, Dongxu Zhao,

https://doi.org/10.18632/aging.102436 pp 10814—10825

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Zhao K, Zhang Y, Yuan H, Zhao M, Zhao D, . Long noncoding RNA LINC00958 accelerates the proliferation and matrix degradation of the nucleus pulposus by regulating miR-203/SMAD3. . 11:10814-10825. https://doi.org/10.18632/aging.102436

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                TY  - JOUR
                AU  - Zhao, Kunchi 
                AU  - Zhang, Yang 
                AU  - Yuan, Hongping 
                AU  - Zhao, Mingming 
                AU  - Zhao, Dongxu 
                TI  - Long noncoding RNA LINC00958 accelerates the proliferation and matrix degradation of the nucleus pulposus by regulating miR-203/SMAD3
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102436
                DO  - 10.18632/aging.102436
                SP  - 10814
                EP  - 10825
                PY  - 
                AB  - Emerging evidence suggests that long noncoding RNAs (lncRNAs) play important roles in the development of intervertebral disc degeneration (IDD). LncRNA LINC00958 has recently been shown to play crucial roles in the development of tumors. However, the role of LINC00958 in IDD remains unclear. We showed that the expression of lncRNA LINC00958 was upregulated in degenerative NP samples, and LINC00958 expression increased gradually along with the grade of exacerbation of disc degeneration. Ectopic expression of LINC00958 promoted nucleus pulposus (NP) cell proliferation, inhibited aggrecan and Col II expression and promoted MMP-2 and MMP-13 expression. In addition, we showed that miR-203 expression was downregulated in degenerative NP samples, and miR-203 expression reduced gradually along with the grade of exacerbation of disc degeneration. Moreover, we demonstrated that the expression of miR-203 was inversely related with LINC00958 expression in NP samples. Ectopic expression of miR-203 inhibited NP cell growth and inhibited ECM degradation. Furthermore, we showed that ectopic expression of miR-203 suppressed the luciferase activity of the wild-type LINC00958 3&apos;-UTR but not the mutant LINC00958 3&apos;-UTR. Elevated expression of LINC00958 inhibited the expression of miR-203 and promoted the expression of SMAD3. In addition, we demonstrated that lncRNA LINC00958 exerted its function by targeting miR-203 in the NP cells. These data suggested that dysregulated lncRNA LINC00958 expression might play an important role in the development of IDD.
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circ5912 suppresses cancer progression via inducing MET in bladder cancer

Yinjie Su, Zehu Du, Guanglei Zhong, Yiyao Ya, Junming Bi, Juanyi Shi, Luping Chen, Wen Dong, Tianxin Lin,

https://doi.org/10.18632/aging.102464 pp 10826—10838

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Su Y, Du Z, Zhong G, Ya Y, Bi J, Shi J, Chen L, Dong W, Lin T, . circ5912 suppresses cancer progression via inducing MET in bladder cancer. . 11:10826-10838. https://doi.org/10.18632/aging.102464

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                TY  - JOUR
                AU  - Su, Yinjie 
                AU  - Du, Zehu 
                AU  - Zhong, Guanglei 
                AU  - Ya, Yiyao 
                AU  - Bi, Junming 
                AU  - Shi, Juanyi 
                AU  - Chen, Luping 
                AU  - Dong, Wen 
                AU  - Lin, Tianxin 
                TI  - circ5912 suppresses cancer progression via inducing MET in bladder cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102464
                DO  - 10.18632/aging.102464
                SP  - 10826
                EP  - 10838
                PY  - 
                AB  - Background: Increasing evidence suggests that circular RNAs play a key role in regulating bladder cancer progression. However, this remains to be fully elucidated.Results: In this study, we reanalyzed our previous RNA sequence, and circ5912 was found to downregulate significantly in bladder cancer tissues compared with normal control. Expression of circ5912 inversely correlates with bladder cancer grade, stage, metastasis, and better patient outcomes. In vitro and in vivo, circ5912 has been shown to repress transforming growth factor &#x3B2; signaling, which suppresses proliferation, invasion and migration of bladder cancer induced by mesenchymal-to epithelial transition.Conclusions: Our study firstly demonstrate that circ5912 regulates mesenchymal-to epithelial transition pathway to suppress bladder cancer progression and propose new therapeutic targets and biomarkers for bladder cancer.Materials and Methods: Clinical values of circ5912 in human bladder cancer were examined in a cohort of 58 patients by qPCR. 2 bladder cancer cell lines, T24 and SW780, were used for biological evaluation of circ5912. CCK8, clone formation, wound healing and trans-well assays were performed to determine the in vivo effect of circ5912; a mouse subcutaneous model was designed for in vivo analysis. Western blotting, RNA pulldown assays and florescent in situ hybridization were applied for mechanistic analysis.
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HIF-2α upregulation mediated by hypoxia promotes NAFLD-HCC progression by activating lipid synthesis via the PI3K-AKT-mTOR pathway

Jianxu Chen, Jiandi Chen, Jiaxin Huang, Zhanyu Li, Yihang Gong, Baojia Zou, Xialei Liu, Lei Ding, Peiping Li, Zhiquan Zhu, Baimeng Zhang, Hui Guo, Chaonong Cai, Jian Li,

https://doi.org/10.18632/aging.102488 pp 10839—10860

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Chen J, Chen J, Huang J, Li Z, Gong Y, Zou B, Liu X, Ding L, Li P, Zhu Z, Zhang B, Guo H, Cai C, et al, . HIF-2α upregulation mediated by hypoxia promotes NAFLD-HCC progression by activating lipid synthesis via the PI3K-AKT-mTOR pathway. . 11:10839-10860. https://doi.org/10.18632/aging.102488

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                TY  - JOUR
                AU  - Chen, Jianxu 
                AU  - Chen, Jiandi 
                AU  - Huang, Jiaxin 
                AU  - Li, Zhanyu 
                AU  - Gong, Yihang 
                AU  - Zou, Baojia 
                AU  - Liu, Xialei 
                AU  - Ding, Lei 
                AU  - Li, Peiping 
                AU  - Zhu, Zhiquan 
                AU  - Zhang, Baimeng 
                AU  - Guo, Hui 
                AU  - Cai, Chaonong 
                AU  - Li, Jian 
                TI  - HIF-2α upregulation mediated by hypoxia promotes NAFLD-HCC progression by activating lipid synthesis via the PI3K-AKT-mTOR pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102488
                DO  - 10.18632/aging.102488
                SP  - 10839
                EP  - 10860
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Chen, Jianxu 
                AU  - Chen, Jiandi 
                AU  - Huang, Jiaxin 
                AU  - Li, Zhanyu 
                AU  - Gong, Yihang 
                AU  - Zou, Baojia 
                AU  - Liu, Xialei 
                AU  - Ding, Lei 
                AU  - Li, Peiping 
                AU  - Zhu, Zhiquan 
                AU  - Zhang, Baimeng 
                AU  - Guo, Hui 
                AU  - Cai, Chaonong 
                AU  - Li, Jian 
                TI  - HIF-2α upregulation mediated by hypoxia promotes NAFLD-HCC progression by activating lipid synthesis via the PI3K-AKT-mTOR pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102488
                DO  - 10.18632/aging.102488
                SP  - 10839
                EP  - 10860
                PY  - 
                AB  - Non-alcoholic fatty liver disease (NAFLD) is a relevant risk factor for developing hepatocellular carcinoma (HCC). Steatohepatitic HCC (SH-HCC), characterized by HCC with steatosis, is influenced by lipid metabolism disorders. A hypoxic microenvironment is common in HCC and affects lipid metabolism. However, whether hypoxia-induced HIF-2&#x3B1; upregulation exacerbates lipid accumulation to contribute to SH-HCC progression remains unclear. In this study, we demonstrated that HIF-2&#x3B1; was elevated in tissues from NAFLD-HCC patients and was associated with survival. Under hypoxic conditions, upregulated HIF-2&#x3B1; was accompanied by lipid accumulation and PI3K-AKT-mTOR pathway activation. HIF-2&#x3B1; knockdown (KD) in steatotic HCC ameliorated triglyceride accumulation and steatosis. HIF-2&#x3B1;-KD steatotic HCC showed minimal lipid synthesis in a hypoxic environment, which contributes to a reduction in malignant behaviours. However, treatment with MHY1485 restored these behaviours. STAM mice, a mouse model that develops NAFLD-HCC, exhibit more rapid tumour progression upon exposure to hypoxia. STAM mice treated with INK-128 presented abrogated mTOR expression and tumour progression under hypoxic conditions with lower triglycerides and steatosis. In conclusion, in a hypoxic microenvironment, HIF-2&#x3B1; upregulation promotes steatotic HCC progression by activating lipid synthesis via the PI3K-AKT-mTOR pathway. Therefore, HIF-2&#x3B1; can be a biomarker and target in developing specific therapeutic measures for NAFLD-HCC patients.
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Glycolysis gene expression profilings screen for prognostic risk signature of hepatocellular carcinoma

Longyang Jiang, Lan Zhao, Jia Bi, Qiutong Guan, Aoshuang Qi, Qian Wei, Miao He, Minjie Wei, Lin Zhao,

https://doi.org/10.18632/aging.102489 pp 10861—10882

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Jiang L, Zhao L, Bi J, Guan Q, Qi A, Wei Q, He M, Wei M, Zhao L, . Glycolysis gene expression profilings screen for prognostic risk signature of hepatocellular carcinoma. . 11:10861-10882. https://doi.org/10.18632/aging.102489

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                TY  - JOUR
                AU  - Jiang, Longyang 
                AU  - Zhao, Lan 
                AU  - Bi, Jia 
                AU  - Guan, Qiutong 
                AU  - Qi, Aoshuang 
                AU  - Wei, Qian 
                AU  - He, Miao 
                AU  - Wei, Minjie 
                AU  - Zhao, Lin 
                TI  - Glycolysis gene expression profilings screen for prognostic risk signature of hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102489
                DO  - 10.18632/aging.102489
                SP  - 10861
                EP  - 10882
                PY  - 
                AB  - Metabolic changes are the markers of cancer and have attracted wide attention in recent years. One of the main metabolic features of tumor cells is the high level of glycolysis, even if there is oxygen. The transformation and preference of metabolic pathways is usually regulated by specific gene expression. The aim of this study is to develop a glycolysis-related risk signature as a biomarker via four common cancer types. Only hepatocellular carcinoma was shown the strong relationship with glycolysis. The mRNA sequencing and chip data of hepatocellular carcinoma, breast invasive carcinoma, renal clear cell carcinoma, colorectal adenocarcinoma were included in the study. Gene set enrichment analysis was performed, profiling three glycolysis-related gene sets, it revealed genes associated with the biological process. Univariate and multivariate Cox proportional regression models were used to screen out prognostic-related gene signature. We identified six mRNAs (DPYSL4, HOMER1, ABCB6, CENPA, CDK1, STMN1) significantly associated with overall survival in the Cox proportional regression model for hepatocellular carcinoma. Based on this gene signature, we were able to divide patients into high-risk and low-risk subgroups. Multivariate Cox regression analysis showed that prognostic power of this six gene signature is independent of clinical variables. Further, we validated this data in our own 55 paired hepatocellular carcinoma and adjacent tissues. The results showed that these proteins were highly expressed in hepatocellular carcinoma tissues compared with adjacent tissue. The survival time of high-risk group was significantly shorter than that of low-risk group, indicating that high-risk group had poor prognosis. We calculated the correlation coefficients between six proteins and found that these six proteins were independent of each other. In conclusions, we developed a glycolysis-related gene signature that could predict survival in hepatocellular carcinoma patients. Our findings provide novel insight to the mechanisms of glycolysis and it is useful for identifying patients with hepatocellular carcinoma with poor prognoses.
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Clinical and transcriptional signatures of human CD204 reveal an applicable marker for the protumor phenotype of tumor-associated macrophages in breast cancer

Yunjie He, Siying Zhou, Fei Deng, Shujie Zhao, Wenquan Chen, Dandan Wang, Xiu Chen, Juncheng Hou, Jian Zhang, Wei Zhang, Li Ding, Jinhai Tang, Zuomin Zhou,

https://doi.org/10.18632/aging.102490 pp 10883—10901

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He Y, Zhou S, Deng F, Zhao S, Chen W, Wang D, Chen X, Hou J, Zhang J, Zhang W, Ding L, Tang J, Zhou Z, . Clinical and transcriptional signatures of human CD204 reveal an applicable marker for the protumor phenotype of tumor-associated macrophages in breast cancer. . 11:10883-10901. https://doi.org/10.18632/aging.102490

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                TY  - JOUR
                AU  - He, Yunjie 
                AU  - Zhou, Siying 
                AU  - Deng, Fei 
                AU  - Zhao, Shujie 
                AU  - Chen, Wenquan 
                AU  - Wang, Dandan 
                AU  - Chen, Xiu 
                AU  - Hou, Juncheng 
                AU  - Zhang, Jian 
                AU  - Zhang, Wei 
                AU  - Ding, Li 
                AU  - Tang, Jinhai 
                AU  - Zhou, Zuomin 
                TI  - Clinical and transcriptional signatures of human CD204 reveal an applicable marker for the protumor phenotype of tumor-associated macrophages in  breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102490
                DO  - 10.18632/aging.102490
                SP  - 10883
                EP  - 10901
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - He, Yunjie 
                AU  - Zhou, Siying 
                AU  - Deng, Fei 
                AU  - Zhao, Shujie 
                AU  - Chen, Wenquan 
                AU  - Wang, Dandan 
                AU  - Chen, Xiu 
                AU  - Hou, Juncheng 
                AU  - Zhang, Jian 
                AU  - Zhang, Wei 
                AU  - Ding, Li 
                AU  - Tang, Jinhai 
                AU  - Zhou, Zuomin 
                TI  - Clinical and transcriptional signatures of human CD204 reveal an applicable marker for the protumor phenotype of tumor-associated macrophages in  breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102490
                DO  - 10.18632/aging.102490
                SP  - 10883
                EP  - 10901
                PY  - 
                AB  - Background: Tumor-associated macrophages in human breast cancer are poorly understood. Specific tumor-associated macrophage-related molecular mechanisms among different intrinsic molecular subtypes remain unclear. Here, we have identified and explored the roles of the tumor-associated macrophages novel marker: CD204 in different subtypes of breast cancer.Results: CD204 was upregulated in four subtypes of breast cancer, and this was associated with poor survival outcomes. CD204 could promote tumor cell proliferation, migration, and invasion and was involved in immune system-related pathways among all subtypes. Special pathways in each subtype were also found. High CD204 mRNA expressions were associated with high proportions of protumor immune cell populations, and most immunoinhibitors positive correlated with CD204 expression in all subtypes.Conclusions: These findings contribute to a better understanding and managing the protumor phenotype of tumor-associated macrophages in different subtypes of breast cancer.Methods: The expression of CD204 and its clinical outcome were analyzed. The roles of CD204 in the regulation of tumor cell proliferation, migration, and invasion were studied. Potential pathways influenced by CD204 were displayed. Immune cell infiltration in different CD204 mRNA expression status and correlations between CD204 and immunoinhibitors were also analyzed.
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The long non-coding RNA SNHG12 promotes gastric cancer by activating the phosphatidylinositol 3-kinase/AKT pathway

Rui Zhang, Yuan Liu, Hui Liu, Wei Chen, Hui-Ning Fan, Jing Zhang, Jin-Shui Zhu,

https://doi.org/10.18632/aging.102493 pp 10902—10922

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Zhang R, Liu Y, Liu H, Chen W, Fan H, Zhang J, Zhu J, . The long non-coding RNA SNHG12 promotes gastric cancer by activating the phosphatidylinositol 3-kinase/AKT pathway. . 11:10902-10922. https://doi.org/10.18632/aging.102493

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Provider: 
 TY - JOUR
 AU - Zhang, Rui 
 AU - Liu, Yuan 
 AU - Liu, Hui 
 AU - Chen, Wei 
 AU - Fan, Hui-Ning 
 AU - Zhang, Jing 
 AU - Zhu, Jin-Shui 
 TI - The long non-coding RNA SNHG12 promotes gastric cancer by activating the phosphatidylinositol 3-kinase/AKT pathway
 JO - 
 JA - 
 VL - 11
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102493
 DO - 10.18632/aging.102493
 SP - 10902
 EP - 10922
 PY - 
 AB - Long non-coding RNAs contribute to the development of human cancers. We compared the long non-coding RNA levels in gastric cancer (GC) and para-cancerous tissues in the Gene Expression Omnibus, and found that small nucleolar RNA host gene 12 (SNHG12) was upregulated in GC tissues. Fluorescence in situ hybridization confirmed that SNHG12 is overexpressed in GC tissues. We then used data from The Cancer Genome Atlas to assess the association of SNHG12 expression with the clinicopathological characteristics and prognosis of GC patients and found that higher SNHG12 expression was associated with a greater tumor invasion depth and poorer survival. In vitro, silencing SNHG12 suppressed GC cell proliferation, migration and invasion, but induced apoptosis and cell cycle arrest. Overexpressing SNHG12 had the opposite effects. In xenografted mice, knocking down SNHG12 reduced GC tumor growth. Taken together, cancer pathway microarray and bioinformatics analyses, RNA pulldown assays, Western blotting and immunohistochemistry revealed that SNHG12 induces GC tumorigenesis by activating the phosphatidylinositol 3-kinase/AKT pathway. SNHG12 may thus be a useful marker for predicting poor survival in GC patients.
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Kainic acid hyperphosphorylates tau via inflammasome activation in MAPT transgenic mice

Xiang-Yu Zheng, Yu-Dan Lv, Feng-Yan Jin, Xiu-Juan Wu, Jie Zhu, Yang Ruan,

https://doi.org/10.18632/aging.102495 pp 10923—10938

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Zheng X, Lv Y, Jin F, Wu X, Zhu J, Ruan Y, . Kainic acid hyperphosphorylates tau via inflammasome activation in MAPT transgenic mice. . 11:10923-10938. https://doi.org/10.18632/aging.102495

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                TY  - JOUR
                AU  - Zheng, Xiang-Yu 
                AU  - Lv, Yu-Dan 
                AU  - Jin, Feng-Yan 
                AU  - Wu, Xiu-Juan 
                AU  - Zhu, Jie 
                AU  - Ruan, Yang 
                TI  - Kainic acid hyperphosphorylates tau via inflammasome activation in MAPT transgenic mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102495
                DO  - 10.18632/aging.102495
                SP  - 10923
                EP  - 10938
                PY  - 
                AB  - The excitotoxicity induced by kainic acid (KA) is thought to contribute to the development of Alzheimer&#x2019;s disease (AD); however, the mechanisms underlying this excitotoxicity remain unknown. In the current study, we investigated the dynamic changes in tau phosphorylation and their associations with the excitotoxicity induced by intraperitoneal injection of KA in the mouse brain. We found that KA-induced excitotoxicity led to sustained hyperphosphorylation of tau in MAPT transgenic (Tg) mice. By using cultured microglia and mouse brains, we showed that KA treatment specifically induced endoplasmic reticulum (ER) stress, which was characterized by activation of the major biomarkers of ER, such as ATF6, GRP78, and IRE1, and resulted in stimulation of inflammasomes. KA receptors (KARs), such as Girk1, were determined to be involved in this KA-induced ER stress. ER stress was also shown to activate inflammasomes by stimulating the expression of the two major components of inflammasomes, nucleotide binding oligomerization domain (NOD)-like receptor (NLR) protein 3 (NLRP3) and nuclear factor (NF)-&#x3BA;B, and eventually causing the production of interleukin-1&#x3B2; (IL-1&#x3B2;). Inhibition of NLRP3 or NF-&#x3BA;B by Bay11-7082 resulted in reduction of KA-induced IL-1&#x3B2; production. Our results also revealed the positive effects of IL-1&#x3B2; on tau phosphorylation, which was blocked by Bay11-7082. Notably, the results indicate that Bay11-7082 acts against KA-induced neuronal degeneration, tau phosphorylation, and memory defects via inflammasomes, which further highlight the protective role of Bay11-7082 in KA-induced neuronal defects.
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Metabolically healthy obesity reduces the risk of Alzheimer’s disease in elders: a longitudinal study

Ling-Zhi Ma, Yu-Yuan Huang, Zuo-Teng Wang, Jie-Qiong Li, Xiao-He Hou, Xue-Ning Shen, Ya-Nan Ou, Qiang Dong, Lan Tan, Jin-Tai Yu, Alzheimer’s Disease Neuroimaging Initiative,

https://doi.org/10.18632/aging.102496 pp 10939—10951

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Ma L, Huang Y, Wang Z, Li J, Hou X, Shen X, Ou Y, Dong Q, Tan L, Yu J, Initiative ADN, . Metabolically healthy obesity reduces the risk of Alzheimer’s disease in elders: a longitudinal study. . 11:10939-10951. https://doi.org/10.18632/aging.102496

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                TY  - JOUR
                AU  - Ma, Ling-Zhi 
                AU  - Huang, Yu-Yuan 
                AU  - Wang, Zuo-Teng 
                AU  - Li, Jie-Qiong 
                AU  - Hou, Xiao-He 
                AU  - Shen, Xue-Ning 
                AU  - Ou, Ya-Nan 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - Yu, Jin-Tai 
                AU  - Initiative, Alzheimer’s Disease Neuroimaging 
                TI  - Metabolically healthy obesity reduces the risk of Alzheimer’s disease in elders: a longitudinal study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102496
                DO  - 10.18632/aging.102496
                SP  - 10939
                EP  - 10951
                PY  - 
                AB  - A subgroup of overweight/obese individuals, who had favorable metabolic profiles, was termed as metabolically healthy overweight/obese (MHO). Several studies suggested that MHO individuals were not at increased risk of cardiovascular disease and all-course mortality. However, whether MHO is associated with excess risk of Alzheimer&#x2019;s disease (AD) in elders remains unclear. To explore the risk of AD among MHO phenotype and investigate whether MHO associates with neurodegenerative biomarkers of AD, we assessed body mass index-metabolic status phenotypes of 1199 longitudinal elders from the Alzheimer&#x2019;s Disease Neuroimaging Initiative (ADNI) cohort using the Adult Treatment Panel-III (ATP- III) criteria. MHO subjects were at a significantly decreased risk for AD (adjusted HR=0.73, 95% CI: 0.54-0.97) compared with metabolically healthy normal weight (MHNW) subjects. In multivariable linear regression models, the cross-sectional associations of MHO with cerebrospinal fluid (CSF) biomarkers, brain A&#x3B2; load, and cortical structure were explored. MHO was positively correlated with CSF-A&#x3B2; (&#x3B2;=0.746, P=0.015), hippocampal volume (&#x3B2;=0.181, P=0.011), and whole brain volume (&#x3B2;=0.133, P=0.004). The MHO phenotype of the elder conferred a decreased risk of AD and its role may be driven by A&#x3B2;.
                ER  -

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Global, regional, and national prevalence and disability-adjusted life-years for infertility in 195 countries and territories, 1990–2017: results from a global burden of disease study, 2017

Hui Sun, Ting-Ting Gong, Yu-Ting Jiang, Shuang Zhang, Yu-Hong Zhao, Qi-Jun Wu,

https://doi.org/10.18632/aging.102497 pp 10952—10991

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Sun H, Gong T, Jiang Y, Zhang S, Zhao Y, Wu Q, . Global, regional, and national prevalence and disability-adjusted life-years for infertility in 195 countries and territories, 1990–2017: results from a global burden of disease study, 2017. . 11:10952-10991. https://doi.org/10.18632/aging.102497

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                TY  - JOUR
                AU  - Sun, Hui 
                AU  - Gong, Ting-Ting 
                AU  - Jiang, Yu-Ting 
                AU  - Zhang, Shuang 
                AU  - Zhao, Yu-Hong 
                AU  - Wu, Qi-Jun 
                TI  - Global, regional, and national prevalence and disability-adjusted life-years for infertility in 195 countries and territories, 1990–2017: results from a global burden of disease study, 2017
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102497
                DO  - 10.18632/aging.102497
                SP  - 10952
                EP  - 10991
                PY  - 
                AB  - To provide comprehensive estimates of the global, regional, and national burden of infertility from 1990 to 2017, using findings from a 2017 study on the global burden of disease (GBD), we assessed the burden of infertility in 195 countries and territories from 1990 to 2017. DisMod-MR 2.1 is a Bayesian meta-regression method that estimates non-fatal outcomes using sparse and heterogeneous epidemiological data. Globally, the age-standardized prevalence rate of infertility increased by 0.370% per year for females and 0.291% per year for males from 1990 to 2017. Additionally, age-standardized disability-adjusted life-years (DALYs) of infertility increased by 0.396% per year for females and 0.293% per year for males during the observational period. An increasing trend to these burden estimates was observed throughout the all socio-demographic index (SDI) countries. Interestingly, we found that high SDI countries had the lowest level of prevalence and DALYs in both genders. However, the largest increasing trend was observed in high-SDI countries for females. By contrast, low-SDI countries had the largest increasing trend in males. Negative associations were observed between these burden estimates and the SDI level. The global disease burden of infertility has been increasing throughout the period from 1990 to 2017.
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Mangiferin promotes macrophage cholesterol efflux and protects against atherosclerosis by augmenting the expression of ABCA1 and ABCG1

Kun Ren, Heng Li, Hui-Fang Zhou, Yin Liang, Min Tong, Lu Chen, Xi-Long Zheng, Guo-Jun Zhao,

https://doi.org/10.18632/aging.102498 pp 10992—11009

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Ren K, Li H, Zhou H, Liang Y, Tong M, Chen L, Zheng X, Zhao G, . Mangiferin promotes macrophage cholesterol efflux and protects against atherosclerosis by augmenting the expression of ABCA1 and ABCG1. . 11:10992-11009. https://doi.org/10.18632/aging.102498

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                TY  - JOUR
                AU  - Ren, Kun 
                AU  - Li, Heng 
                AU  - Zhou, Hui-Fang 
                AU  - Liang, Yin 
                AU  - Tong, Min 
                AU  - Chen, Lu 
                AU  - Zheng, Xi-Long 
                AU  - Zhao, Guo-Jun 
                TI  - Mangiferin promotes macrophage cholesterol efflux and protects against atherosclerosis by augmenting the expression of ABCA1 and ABCG1
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102498
                DO  - 10.18632/aging.102498
                SP  - 10992
                EP  - 11009
                PY  - 
                AB  - Mangiferin has been identified as a potent cardioprotective factor that enhances high-density lipoprotein cholesterol levels in plasma. The aim of this study was to investigate the impact of mangiferin on macrophage cholesterol efflux and the development of atherosclerosis. The results showed that mangiferin injection significantly decreased atherosclerotic plaque size, and reduced plasma levels of low-density lipoprotein cholesterol, triglyceride, and total cholesterol in apoE knockout mice, whereas reverse cholesterol transport efficiency and high-density lipoprotein cholesterol levels were enhanced. In vitro study showed that mangiferin prevented lipid accumulation and promoted [3H]-cholesterol efflux from acetylated LDL-loaded RAW264.7 macrophages with an increase in the expression of ATP binding cassette A1/G1 (ABCA1/G1), liver X receptor-&#x3B1; (LXR&#x3B1;) and peroxisome proliferator-activated receptor-&#x3B3; (PPAR&#x3B3;). Moreover, transfection of PPAR&#x3B3; siRNA or LXR&#x3B1; siRNA markedly abolished the positive effects of mangiferin on ABCA1/G1 expression and cholesterol efflux. The opposite effects were observed after treatment with PPAR&#x3B3; agonist rosiglitazone or LXR&#x3B1; agonist T0901317. In conclusion, mangiferin may attenuate atherogenesis by promoting cholesterol efflux from macrophages via the PPAR&#x3B3;-LXR&#x3B1;-ABCA1/G1 pathway.
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Reactive oxygen species metabolism-based prediction model and drug for patients with recurrent glioblastoma

Nian Tan, Jianwei Liu, Ping Li, Zhaoying Sun, Jianming Pan, Wei Zhao,

https://doi.org/10.18632/aging.102506 pp 11010—11029

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Tan N, Liu J, Li P, Sun Z, Pan J, Zhao W, . Reactive oxygen species metabolism-based prediction model and drug for patients with recurrent glioblastoma. . 11:11010-11029. https://doi.org/10.18632/aging.102506

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                TY  - JOUR
                AU  - Tan, Nian 
                AU  - Liu, Jianwei 
                AU  - Li, Ping 
                AU  - Sun, Zhaoying 
                AU  - Pan, Jianming 
                AU  - Zhao, Wei 
                TI  - Reactive oxygen species metabolism-based prediction model and drug for patients with recurrent  glioblastoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102506
                DO  - 10.18632/aging.102506
                SP  - 11010
                EP  - 11029
                PY  - 
                AB  - Background: Tumor recurrence is the main cause of poor prognosis of GBM. Finding the characteristics of recurrent GBM that provide early warning of tumor recurrence can provide guidance for the clinical treatment of recurrent GBM.Results: Reactive oxygen species (ROS) biosynthetic processes was significantly elevated in recurrent GBM. The recurrent risk score based on the ROS biosynthetic process was closely related to tumor purity and tumor immune functions. The quantitative risk assessment system could be used to predict the recurrence time of GBM. Gallic acid, a compound with high anti-oxidation activity and low cytotoxicity, was screened as a potential chemotherapy sensitizer for recurrent GBM.Conclusion: The quantitative risk assessment system based on ROS biosynthetic process could be used for early warning of GBM recurrence. Combination of low-dose gallic acid and temozolomide could improve therapeutic outcomes in recurrent GBM.Methods: A total of 663 primary and recurrent GBM samples with clinical and microarray data were included in this study. GSVA, LASSO-COX, and Kaplan-Meier survive curve were performed to construct and verify a quantitative risk assessment system for GBM recurrence prediction. An antioxidant capacity test and cell viability test were used to discover potential drugs for recurrent GBM.
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Parity is associated with albuminuria and chronic kidney disease: a population-based study

Kan Sun, Diaozhu Lin, Qiling Feng, Feng Li, Yiqin Qi, Chulin Huang, Wanting Feng, Chuan Yang, Li Yan, Meng Ren,

https://doi.org/10.18632/aging.102507 pp 11030—11039

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Sun K, Lin D, Feng Q, Li F, Qi Y, Huang C, Feng W, Yang C, Yan L, Ren M, . Parity is associated with albuminuria and chronic kidney disease: a population-based study. . 11:11030-11039. https://doi.org/10.18632/aging.102507

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                TY  - JOUR
                AU  - Sun, Kan 
                AU  - Lin, Diaozhu 
                AU  - Feng, Qiling 
                AU  - Li, Feng 
                AU  - Qi, Yiqin 
                AU  - Huang, Chulin 
                AU  - Feng, Wanting 
                AU  - Yang, Chuan 
                AU  - Yan, Li 
                AU  - Ren, Meng 
                TI  - Parity is associated with albuminuria and chronic kidney disease: a population-based study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102507
                DO  - 10.18632/aging.102507
                SP  - 11030
                EP  - 11039
                PY  - 
                AB  - Background and aims: Epidemiological studies have shown that increasing parity is associated with risk of hypertension and diabetes in parous women. However, the relationship between the parity degree with chronic kidney disease (CKD) is still unknown.Results: Parous women with higher parity had increased age, body mass index, waist circumference, systolic blood pressure, fasting plasma glucose, fasting insulin and decreased high-density lipoprotein cholesterol, eGFR and education levels. Compared with women with one-child birth, those with more than two-child births had greater prevalence of increased urinary albumin excretion (odds ratios [ORs] 1.53, 95% confidence intervals [CI], 1.03 - 2.28) and CKD (ORs 1.79, 95% CI, 1.24 - 2.58) after multiple adjustments. In dose-response analysis, a nonlinear relationship of parity degree with albuminuria and CKD was detected.Conclusion: Parity is associated with higher prevalence of albuminuria and CKD in middle-aged and elderly Chinese women.Methods: We conducted a community-based study in 6,946 women to investigate the association of parity with albuminuria and CKD. Increased urinary albumin excretion was defined as albumin-to-creatinine ratio (ACR) greater or equal than 30 mg/g. CKD was defined as estimated glomerular filtration rate (eGFR) less than 60 mL/min per 1.73 m&#xB2; or presence of albuminuria.
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Sphingosine-1-phosphate promotes PDGF-dependent endothelial progenitor cell angiogenesis in human chondrosarcoma cells

Chao-Qun Wang, Chih-Yang Lin, Yuan-Li Huang, Shih-Wei Wang, Yan Wang, Bi-Fei Huang, Yu-Wei Lai, Shun-Long Weng, Yi-Chin Fong, Chih-Hsin Tang, Zhong Lv,

https://doi.org/10.18632/aging.102508 pp 11040—11053

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Wang C, Lin C, Huang Y, Wang S, Wang Y, Huang B, Lai Y, Weng S, Fong Y, Tang C, Lv Z, . Sphingosine-1-phosphate promotes PDGF-dependent endothelial progenitor cell angiogenesis in human chondrosarcoma cells. . 11:11040-11053. https://doi.org/10.18632/aging.102508

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                TY  - JOUR
                AU  - Wang, Chao-Qun 
                AU  - Lin, Chih-Yang 
                AU  - Huang, Yuan-Li 
                AU  - Wang, Shih-Wei 
                AU  - Wang, Yan 
                AU  - Huang, Bi-Fei 
                AU  - Lai, Yu-Wei 
                AU  - Weng, Shun-Long 
                AU  - Fong, Yi-Chin 
                AU  - Tang, Chih-Hsin 
                AU  - Lv, Zhong 
                TI  - Sphingosine-1-phosphate promotes PDGF-dependent endothelial progenitor cell angiogenesis in human chondrosarcoma cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102508
                DO  - 10.18632/aging.102508
                SP  - 11040
                EP  - 11053
                PY  - 
                AB  - The malignant bone tumors that are categorized as chondrosarcomas display a high potential for metastasis in late-stage disease. Higher-grade chondrosarcomas contain higher levels of expression of platelet-derived growth factor (PDGF) and its receptor. The phosphorylation of sphingosine by sphingosine kinase enzymes SphK1 and SphK2 generates sphingosine-1-phosphate (S1P), which inhibits human chondrosarcoma cell migration, while SphK1 overexpression suppresses lung metastasis of chondrosarcoma. We sought to determine whether S1P mediates levels of PDGF-A expression and angiogenesis in chondrosarcoma. Surprisingly, our investigations found that treatment of chondrosarcoma cells with S1P and transfecting them with SphK1 cDNA increased PDGF-A expression and induced angiogenesis of endothelial progenitor cells (EPCs). Ras, Raf, MEK, ERK and AP-1 inhibitors and their small interfering RNAs (siRNAs) inhibited S1P-induced PDGF-A expression and EPC angiogenesis. Our results indicate that S1P promotes the expression of PDGF-A in chondrosarcoma via the Ras/Raf/MEK/ERK/AP-1 signaling cascade and stimulates EPC angiogenesis.
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EGFR-specific CAR-T cells trigger cell lysis in EGFR-positive TNBC

Yan Liu, Yehui Zhou, Kuo-Hsiang Huang, Ying Li, Xujie Fang, Li An, Feifei Wang, Qingfei Chen, Yunchao Zhang, Aihua Shi, Shuang Yu, Jingzhong Zhang,

https://doi.org/10.18632/aging.102510 pp 11054—11072

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Liu Y, Zhou Y, Huang K, Li Y, Fang X, An L, Wang F, Chen Q, Zhang Y, Shi A, Yu S, Zhang J, . EGFR-specific CAR-T cells trigger cell lysis in EGFR-positive TNBC. . 11:11054-11072. https://doi.org/10.18632/aging.102510

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                TY  - JOUR
                AU  - Liu, Yan 
                AU  - Zhou, Yehui 
                AU  - Huang, Kuo-Hsiang 
                AU  - Li, Ying 
                AU  - Fang, Xujie 
                AU  - An, Li 
                AU  - Wang, Feifei 
                AU  - Chen, Qingfei 
                AU  - Zhang, Yunchao 
                AU  - Shi, Aihua 
                AU  - Yu, Shuang 
                AU  - Zhang, Jingzhong 
                TI  - EGFR-specific CAR-T cells trigger cell lysis in EGFR-positive TNBC
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102510
                DO  - 10.18632/aging.102510
                SP  - 11054
                EP  - 11072
                PY  - 
                AB  - Triple-negative breast cancer (TNBC) is an aggressive cancer subtype for which effective therapies are lacking. Epidermal growth factor receptor (EGFR) is overexpressed in various types of TNBC cells, and several EGFR-specific immunotherapies have been used to treat cancer patients. Chimeric antigen receptor engineered T (CAR-T) cells have also been used as cancer therapies. In this study, we generated two types of EGFR-specific CAR-modified T cells using lentiviral vectors with DNA sequences encoding the scFv regions of two anti-EGFR antibodies. The cytotoxic and antitumor effects of these CAR-modified T cells were examined in cytokine release and cytotoxicity assays in vitro and in tumor growth assays in TNBC cell line- and patient-derived xenograft mouse models. Both types of EGFR-specific CAR-T cells were activated by high-EGFR-expressing TNBC cells and specifically triggered TNBC cell lysis in vitro. Additionally, the CAR-T cells inhibited growth of cell-line- and patient-derived xenograft TNBC tumors in mice. These results suggest that EGFR-specific CAR-T cells might be a promising therapeutic strategy in patients with high-EGFR-expressing TNBC.
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Clinical and neuroimaging correlates among cohorts of cerebral arteriostenosis, venostenosis and arterio-venous stenosis

Jiayue Ding, Jingwei Guan, Gary Rajah, David Dornbos III, Weili Li, Zhongao Wang, Yuchuan Ding, Xunming Ji, Ran Meng,

https://doi.org/10.18632/aging.102511 pp 11073—11083

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Ding J, Guan J, Rajah G, III DD, Li W, Wang Z, Ding Y, Ji X, Meng R, . Clinical and neuroimaging correlates among cohorts of cerebral arteriostenosis, venostenosis and arterio-venous stenosis. . 11:11073-11083. https://doi.org/10.18632/aging.102511

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                TY  - JOUR
                AU  - Ding, Jiayue 
                AU  - Guan, Jingwei 
                AU  - Rajah, Gary 
                AU  - III, David Dornbos 
                AU  - Li, Weili 
                AU  - Wang, Zhongao 
                AU  - Ding, Yuchuan 
                AU  - Ji, Xunming 
                AU  - Meng, Ran 
                TI  - Clinical and neuroimaging correlates among cohorts of cerebral arteriostenosis, venostenosis and arterio-venous stenosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102511
                DO  - 10.18632/aging.102511
                SP  - 11073
                EP  - 11083
                PY  - 
                AB  - The purpose of this study was to discriminate the clinical and imaging correlates of cerebral arterial stenosis (CAS), venous stenosis (CVS) and arterio-venous stenosis (CAVS) in the clinical setting. Patients were classified into three groups: CAS (n = 75), CVS (n=74) and CAVS (n=67). Focal neurological deficits were the prominent presenting symptoms in CAS group, while venous turbulence related symptoms were common in both CVS and CAVS group. Risk factor analysis showed the OR (95%CI) for diabetes, male gender and age in CAS vs. CVS group were 13.67(2.71, 68.85), 6.69(2.39, 18.67) and 1.07(1.03, 1.12) respectively. Male gender, diabetes and age in CAVS vs. CAS groups were 0.27(0.11, 0.63), 0.26(0.10, 0.67) and 1.09(1.04, 1.14) respectively, while age in CAVS vs. CVS group was 1.11(1.07, 1.15). The white matter lesions (WMLs) in CAS group varied in size, with clear boundaries asymmetrically distributed in bilateral hemispheres. CVS-induced WMLs revealed a bilaterally symmetric, cloudy-like appearance. The cerebral perfusion was asymmetrically reduced in CAS but symmetrically reduced in CVS group. The clinical characteristics and neuroimaging presentations were different among patients with CAS, CVS and CAVS. We recommended for aged patients, both arterial and venous imaging should be considered in diagnosis of cerebral stenotic vascular disorders.
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α-Mangostin remodels visceral adipose tissue inflammation to ameliorate age-related metabolic disorders in mice

Dan Li, Qianyu Liu, Xiuqiang Lu, Zhengqiu Li, Chunming Wang, Chung-Hang Leung, Yitao Wang, Cheng Peng, Ligen Lin,

https://doi.org/10.18632/aging.102512 pp 11084—11110

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Li D, Liu Q, Lu X, Li Z, Wang C, Leung C, Wang Y, Peng C, Lin L, . α-Mangostin remodels visceral adipose tissue inflammation to ameliorate age-related metabolic disorders in mice. . 11:11084-11110. https://doi.org/10.18632/aging.102512

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                TY  - JOUR
                AU  - Li, Dan 
                AU  - Liu, Qianyu 
                AU  - Lu, Xiuqiang 
                AU  - Li, Zhengqiu 
                AU  - Wang, Chunming 
                AU  - Leung, Chung-Hang 
                AU  - Wang, Yitao 
                AU  - Peng, Cheng 
                AU  - Lin, Ligen 
                TI  - α-Mangostin remodels visceral adipose tissue inflammation to ameliorate age-related metabolic disorders in mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102512
                DO  - 10.18632/aging.102512
                SP  - 11084
                EP  - 11110
                PY  - 
                AB  - Low-grade chronic adipose tissue inflammation contributes to the onset and development of aging-related insulin resistance and type 2 diabetes. In the current study, &#x3B1;-mangostin, a xanthone isolated from mangosteen (Garcinia mangostana), was identified to ameliorate lipopolysaccharides-induced acute adipose tissue inflammation in mice, by reducing the expression of pro-inflammatory cytokines and chemokines. In a cohort of young (3 months) and old (18&#x2013;20 months) mice, &#x3B1;-mangostin mitigated aging-associated adiposity, hyperlipidemia, and insulin resistance. Further study showed that &#x3B1;-mangostin alleviated aging-related adipose tissue inflammation by reducing macrophage content and shifting pro-inflammatory macrophage polarization. Moreover, &#x3B1;-mangostin protected the old mice against liver injury through suppressing the secretion of microRNA-155-5p from macrophages. The above results demonstrated that &#x3B1;-mangostin represents a new scaffold to alleviate adipose tissue inflammation, which might be a novel candidate to treat aging-related metabolic disorders.
                ER  -

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Daily decrease of post-operative alpha-fetoprotein by 9% discriminates prognosis of HCC: A multicenter retrospective study

Pei-Yun Zhou, Chao-Ping Yang, Zheng Tang, Yong Yi, Wei-Ren Liu, Meng-Xin Tian, Jin-Long Huang, Wei Gan, Xi-Fei Jiang, Gao Liu, Han Wang, Chen-Yang Tao, Yuan Fang, Wei-Feng Qu, Cheng Zhou, Ruo-Yu Guan, Bao-Ye Sun, Yu-Fu Zhou, Shu-Shu Song, Zhen-Bin Ding, Yuan-Fei Peng, Zhi Dai, Jian Zhou, Jia Fan, Guo-Zhong Gong, Ying-Hong Shi, Shuang-Jian Qiu,

https://doi.org/10.18632/aging.102513 pp 11111—11123

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Zhou P, Yang C, Tang Z, Yi Y, Liu W, Tian M, Huang J, Gan W, Jiang X, Liu G, Wang H, Tao C, Fang Y, et al, . Daily decrease of post-operative alpha-fetoprotein by 9% discriminates prognosis of HCC: A multicenter retrospective study. . 11:11111-11123. https://doi.org/10.18632/aging.102513

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                TY  - JOUR
                AU  - Zhou, Pei-Yun 
                AU  - Yang, Chao-Ping 
                AU  - Tang, Zheng 
                AU  - Yi, Yong 
                AU  - Liu, Wei-Ren 
                AU  - Tian, Meng-Xin 
                AU  - Huang, Jin-Long 
                AU  - Gan, Wei 
                AU  - Jiang, Xi-Fei 
                AU  - Liu, Gao 
                AU  - Wang, Han 
                AU  - Tao, Chen-Yang 
                AU  - Fang, Yuan 
                AU  - Qu, Wei-Feng 
                AU  - Zhou, Cheng 
                AU  - Guan, Ruo-Yu 
                AU  - Sun, Bao-Ye 
                AU  - Zhou, Yu-Fu 
                AU  - Song, Shu-Shu 
                AU  - Ding, Zhen-Bin 
                AU  - Peng, Yuan-Fei 
                AU  - Dai, Zhi 
                AU  - Zhou, Jian 
                AU  - Fan, Jia 
                AU  - Gong, Guo-Zhong 
                AU  - Shi, Ying-Hong 
                AU  - Qiu, Shuang-Jian 
                TI  - Daily decrease of post-operative alpha-fetoprotein by 9% discriminates prognosis of HCC: A multicenter retrospective study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102513
                DO  - 10.18632/aging.102513
                SP  - 11111
                EP  - 11123
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhou, Pei-Yun 
                AU  - Yang, Chao-Ping 
                AU  - Tang, Zheng 
                AU  - Yi, Yong 
                AU  - Liu, Wei-Ren 
                AU  - Tian, Meng-Xin 
                AU  - Huang, Jin-Long 
                AU  - Gan, Wei 
                AU  - Jiang, Xi-Fei 
                AU  - Liu, Gao 
                AU  - Wang, Han 
                AU  - Tao, Chen-Yang 
                AU  - Fang, Yuan 
                AU  - Qu, Wei-Feng 
                AU  - Zhou, Cheng 
                AU  - Guan, Ruo-Yu 
                AU  - Sun, Bao-Ye 
                AU  - Zhou, Yu-Fu 
                AU  - Song, Shu-Shu 
                AU  - Ding, Zhen-Bin 
                AU  - Peng, Yuan-Fei 
                AU  - Dai, Zhi 
                AU  - Zhou, Jian 
                AU  - Fan, Jia 
                AU  - Gong, Guo-Zhong 
                AU  - Shi, Ying-Hong 
                AU  - Qiu, Shuang-Jian 
                TI  - Daily decrease of post-operative alpha-fetoprotein by 9% discriminates prognosis of HCC: A multicenter retrospective study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102513
                DO  - 10.18632/aging.102513
                SP  - 11111
                EP  - 11123
                PY  - 
                AB  - Background: Mixed evidence challenges preoperative alpha-fetoprotein (AFP) as an independent prognostic factor for patients with hepatocellular carcinoma (HCC) after hepatectomy.Results: Daily post-operative decrease of AFP by 9% as compared to the preoperative level (A09) were selected as the Cut-off. The Kaplan-Meier curve showed that A09 was significantly different for OS (P=0.043) and RFS (P=0.03). A decrease in risk by 54% was observed for OS and 32% for RFS in the at-risk population (A09&gt;9%). A better concordance was observed after adding A09 into TNM and BCLC staging systems. Moreover, a consistent concordance was observed in the internal (FDZS5:0.63; FDZS3:0.608) and external (FDZS5:0.85; FDZS3:0.762) validation cohorts, suggesting its prognostic value in HCC population with elevated AFP.Conclusions: Decrease in perioperative serum AFP rather than preoperative AFP is an independent prognostic factor for HCC patients after hepatectomy. Cut-off A09 significantly discriminates overall and recurrence-free survival and could be interpret into TNM and BCLC staging systems to improve the stratification power for HCC patients with elevated AFP.Methods: Kaplan-Meier curve depicted the differences of overall survival (OS) and recurrence-free survival (RFS). Nomogram and concordance were employed to evaluate the superiority of the current staging system.
                ER  -

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JAK1 as a prognostic marker and its correlation with immune infiltrates in breast cancer

Bo Chen, Jianguo Lai, Danian Dai, Rong Chen, Xuan Li, Ning Liao,

https://doi.org/10.18632/aging.102514 pp 11124—11135

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Chen B, Lai J, Dai D, Chen R, Li X, Liao N, . JAK1 as a prognostic marker and its correlation with immune infiltrates in breast cancer. . 11:11124-11135. https://doi.org/10.18632/aging.102514

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Provider: 
 TY - JOUR
 AU - Chen, Bo 
 AU - Lai, Jianguo 
 AU - Dai, Danian 
 AU - Chen, Rong 
 AU - Li, Xuan 
 AU - Liao, Ning 
 TI - JAK1 as a prognostic marker and its correlation with immune infiltrates in breast cancer
 JO - 
 JA - 
 VL - 11
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102514
 DO - 10.18632/aging.102514
 SP - 11124
 EP - 11135
 PY - 
 AB - Clinical trials testing Janus kinase-1 (JAK1) inhibitors in cancers are under way. Whether the JAK1 mRNA levels in breast tumors correlates with outcome has not been evaluated. JAK1 expression was analyzed via the Oncomine database and Tumor IMmune Estimation Resource site. Tumor tissues from 57 breast cancer patients were used for qRT-PCR and immune infiltration assessment. JAK1 expression was significantly lower in breast invasive carcinoma compared with adjacent normal tissues. Public databases (Kaplan-Meier plotter and PrognoScan) showed that low JAK1 expression was associated with poorer survival. Data from The Cancer Genome Atlas (TCGA) showed that high JAK1 expression was associated with increased survival in both TNM I-II and TNM III-IV patients. JAK1 was inversely correlated with tumor size status, lymph node status, and TNM of breast cancer patients. JAK1 levels were correlated with the T cell transcript-enriched LYM metagene signature and was significantly lower in the low tumor infiltrating lymphocytes (TILs) group. JAK1 expression levels had significant positive correlations with infiltrating levels of CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells in breast cancer and not with other B cells. In conclusion, JAK1 mRNA levels were correlated with prognosis and immune infiltrating levels in breast cancer.
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Ninjurin2 overexpression promotes glioma cell growth

Li-Na Zhou, Ping Li, Shang Cai, Gang Li, Fang Liu,

https://doi.org/10.18632/aging.102515 pp 11136—11147

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Zhou L, Li P, Cai S, Li G, Liu F, . Ninjurin2 overexpression promotes glioma cell growth. . 11:11136-11147. https://doi.org/10.18632/aging.102515

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                TY  - JOUR
                AU  - Zhou, Li-Na 
                AU  - Li, Ping 
                AU  - Cai, Shang 
                AU  - Li, Gang 
                AU  - Liu, Fang 
                TI  - Ninjurin2 overexpression promotes glioma cell growth
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102515
                DO  - 10.18632/aging.102515
                SP  - 11136
                EP  - 11147
                PY  - 
                AB  - Ninjurin2 (Ninj2) is an adhesion protein expressed in neurons and glial cells. The current study tested its expression and potential functions in human glioma. We show that Ninj2 mRNA and protein levels are significantly upregulated in human glioma cells and tissues. In established and primary human glioma cells, Ninj2 shRNA or knockout (by CRISPR/Cas9 gene editing) potently inhibited cell survival, growth, proliferation, cell migration and invasion, while inducing apoptosis activation. Contrarily, ectopic overexpression of Ninj2 promoted glioma cell progression in vitro. In human glioma tissues and cells, Ninj2 co-immunoprecipitated with multiple receptor tyrosine kinases (EGFR, PDGFR&#x3B2; and FGFR), required for downstream Akt and Erk activation. Akt and Erk activation was potently inhibited by Ninj2 shRNA or knockout, but enhanced with ectopic Ninj2 overexpression in glioma cells. In summary, we show that Ninj2 overexpression promotes glioma cell growth.
                ER  -

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Apolipoprotein E regulates mitochondrial function through the PGC-1α-sirtuin 3 pathway

Junxiang Yin, Megan Nielsen, Tanner Carcione, Shiping Li, Jiong Shi,

https://doi.org/10.18632/aging.102516 pp 11148—11156

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Yin J, Nielsen M, Carcione T, Li S, Shi J, . Apolipoprotein E regulates mitochondrial function through the PGC-1α-sirtuin 3 pathway. . 11:11148-11156. https://doi.org/10.18632/aging.102516

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                TY  - JOUR
                AU  - Yin, Junxiang 
                AU  - Nielsen, Megan 
                AU  - Carcione, Tanner 
                AU  - Li, Shiping 
                AU  - Shi, Jiong 
                TI  - Apolipoprotein E regulates mitochondrial function through the PGC-1α-sirtuin 3 pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102516
                DO  - 10.18632/aging.102516
                SP  - 11148
                EP  - 11156
                PY  - 
                AB  - Cerebral hypometabolism is a pathophysiological hallmark of Alzheimer&#x2019;s disease (AD). Our previous studies found that a mitochondrial protein, sirtuin3 (Sirt3), was down-regulated in human AD postmortem brains. Sirt3 protected neurons against oligo-amyloid &#x3B2;-42 induced hypometabolism in human Apolipoprotein E4 (ApoE4) transgenic mice. However, how ApoE affects mitochondrial function and its proteins such as Sirt3 remains unclear.We characterized and compared levels of Sirt3 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1&#x3B1;, a Sirt3 activator), oxidative stress proteins, synaptic proteins, cognitive task performance and ATP production in 12-month old human ApoE4 and ApoE3 transgenic mice, and assessed changes in Sirt3 expression on cellular metabolism in primary neurons from ApoE4 and ApoE3 transgenic mice.Compared to ApoE3 mice, Sirt3 and PGC-1&#x3B1; levels were significantly lower in ApoE4 mice. Learning and memory, synaptic proteins, the NAD+/ NADH ratios, and ATP production were significantly lower in ApoE4 mice as well. Sirt3 knockdown reduced the oxygen consumption and ATP production in primary neurons with the human ApoE3, while Sirt3 overexpression protected these damages in ApoE4 neurons.Our findings suggest that ApoE4 suppresses mitochondrial function via the PGC-1&#x3B1;- Sirt3 pathway. This discovery provides us novel therapeutic targets for the treatment and prevention of AD.
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A twenty gene-based gene set variation score reflects the pathological progression from cirrhosis to hepatocellular carcinoma

Yan Lin, Rong Liang, Jiazhou Ye, Qian Li, Ziyu Liu, Xing Gao, Xuemin Piao, Rongyun Mai, Donghua Zou, Lianying Ge,

https://doi.org/10.18632/aging.102518 pp 11157—11169

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Lin Y, Liang R, Ye J, Li Q, Liu Z, Gao X, Piao X, Mai R, Zou D, Ge L, . A twenty gene-based gene set variation score reflects the pathological progression from cirrhosis to hepatocellular carcinoma. . 11:11157-11169. https://doi.org/10.18632/aging.102518

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                TY  - JOUR
                AU  - Lin, Yan 
                AU  - Liang, Rong 
                AU  - Ye, Jiazhou 
                AU  - Li, Qian 
                AU  - Liu, Ziyu 
                AU  - Gao, Xing 
                AU  - Piao, Xuemin 
                AU  - Mai, Rongyun 
                AU  - Zou, Donghua 
                AU  - Ge, Lianying 
                TI  - A twenty gene-based gene set variation score reflects the pathological progression from cirrhosis to hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102518
                DO  - 10.18632/aging.102518
                SP  - 11157
                EP  - 11169
                PY  - 
                AB  - The molecular mechanism of the pathological progression from cirrhosis to hepatocellular carcinoma (HCC) remains elusive. In the present study, tissue samples from normal liver, cirrhosis and HCC were subjected to differentially gene expression analysis, weighted gene correlation network analysis to identify the twenty hub genes (TOP2A, CDC20, PTTG1, CDCA5, CCNB2, PRC1, KIF20A, SF3B4, HSP90AB1, FOXD2, PLOD3, CCT3, SETDB1, VPS45, SPDL1, RACGAP1, MED24, KIAA0101, ZNF282, and USP21) in the pathological progression from cirrhosis to HCC. Each sample was calculated a hub gene set variation analysis (HGSVA) score using Gene Set Variation Analysis, The HGSVA score significantly increased with progression from cirrhosis to HCC, and this result was validated in two independent data sets. Moreover, this score may be used as a blood-based marker for HCC and is an independent prognostic factor of recurrence-free survival (RFS) and overall survival (OS). High expression of the hub genes may be driven by hypomethylation. The twenty gene-based gene set variation score may reflect the pathological progression from cirrhosis to HCC and is an independent prognostic factor for both OS and RFS.
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Identification of differentially expressed genes in non-small cell lung cancer

Ke Wang, Ruo Chen, Zhuan Feng, Yu-Meng Zhu, Xiu-Xuan Sun, Wan Huang, Zhi-Nan Chen,

https://doi.org/10.18632/aging.102521 pp 11170—11185

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Wang K, Chen R, Feng Z, Zhu Y, Sun X, Huang W, Chen Z, . Identification of differentially expressed genes in non-small cell lung cancer. . 11:11170-11185. https://doi.org/10.18632/aging.102521

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                TY  - JOUR
                AU  - Wang, Ke 
                AU  - Chen, Ruo 
                AU  - Feng, Zhuan 
                AU  - Zhu, Yu-Meng 
                AU  - Sun, Xiu-Xuan 
                AU  - Huang, Wan 
                AU  - Chen, Zhi-Nan 
                TI  - Identification of differentially expressed genes in non-small cell lung cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102521
                DO  - 10.18632/aging.102521
                SP  - 11170
                EP  - 11185
                PY  - 
                AB  - Lung cancer is the most common malignant tumor and the leading cause of cancer-related deaths worldwide. Because current treatments for advanced non-small cell lung cancer (NSCLC), the most prevalent lung cancer histological subtype, show limited efficacy, screening for tumor-associated biomarkers using bioinformatics reflects the hope to improve early diagnosis and prognosis assessment. In our study, a Gene Expression Omnibus dataset was analyzed to identify genes with prognostic significance in NSCLC. Upon comparison with matched normal tissues, 118 differentially expressed genes (DEGs) were identified in NSCLC, and their functions were explored through bioinformatics analyses. The most significantly upregulated DEGs were TOP2A, SLC2A1, TPX2, and ASPM, all of which were significantly associated with poor overall survival (OS). Further analysis revealed that TOP2A had prognostic significance in early-stage lung cancer patients, and its expression correlated with levels of immune cell infiltration, especially dendritic cells (DCs). Our study provides a dataset of potentially prognostic NSCLC biomarkers, and highlights TOP2A as a valuable survival biomarker to improve prediction of prognosis in NSCLC.
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Active compounds of herbs ameliorate impaired cognition in APP/PS1 mouse model of Alzheimer’s disease

WenJun Yu, ShengJun An, TieMei Shao, HongJun Xu, HongXu Chen, JunDa Ning, YongJie Zhou, XiQing Chai,

https://doi.org/10.18632/aging.102522 pp 11186—11201

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Yu W, An S, Shao T, Xu H, Chen H, Ning J, Zhou Y, Chai X, . Active compounds of herbs ameliorate impaired cognition in APP/PS1 mouse model of Alzheimer’s disease. . 11:11186-11201. https://doi.org/10.18632/aging.102522

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                TY  - JOUR
                AU  - Yu, WenJun 
                AU  - An, ShengJun 
                AU  - Shao, TieMei 
                AU  - Xu, HongJun 
                AU  - Chen, HongXu 
                AU  - Ning, JunDa 
                AU  - Zhou, YongJie 
                AU  - Chai, XiQing 
                TI  - Active compounds of herbs ameliorate impaired cognition in APP/PS1 mouse model of Alzheimer’s disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102522
                DO  - 10.18632/aging.102522
                SP  - 11186
                EP  - 11201
                PY  - 
                AB  - Alzheimer&#x2019;s disease (AD), the most common cause of dementia, is a neurodegenerative disorder characterized by amyloid plaque accumulations, intracellular tangles and neuronal loss in certain brain regions. It has been shown that a disturbance of normal iron metabolism contributes to the pathophysiology of AD. However, the mechanism underlying abnormal iron load in the brain of AD patients is unclear. The frontal cortex, an important brain structure for executive function, is one of the regions affected by AD. We investigated the beneficial effects of active compounds of Epimedium, Astragaoside and Puerarin on iron metabolism in the frontal cortex of six-month-old APPswe/PS1&#x394;E9 (APP/PS1) double transgenic mouse, a model of AD. Treatment with the active compounds reduced cognitive and memory deficits and damaged cell ultrastructure in APP/PS1 mice. These beneficial effects were associated with changes in expression levels of iron metabolism proteins in the frontal cortex, including divalent metal transporter with iron response element (DMT1-with IRE), divalent metal transporter without iron response element (DMT1-without IRE), transferrin (TF) and transferring receptor 1 (TfR1); three release proteins including the exporter ferroportin 1 (Fpn1), ceruloplasmin (CP) and hephaestin (HEPH), one increased storage iron protein ferritin and one iron regulating hormone hepcidin. These findings suggest that the active compounds improve cognition and memory in brain neurodegenerative disorders and these beneficial effects are associated with reduced impairment of iron metabolism. This study may provide a new strategy for developing novel drugs to treat AD.
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ciRs-6 upregulates March1 to suppress bladder cancer growth by sponging miR-653

Yinjie Su, Weilian Feng, Guanglei Zhong, Yiyao Ya, Zehu Du, Juanyi Shi, Luping Chen, Wen Dong, Tianxin Lin,

https://doi.org/10.18632/aging.102525 pp 11202—11223

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Su Y, Feng W, Zhong G, Ya Y, Du Z, Shi J, Chen L, Dong W, Lin T, . ciRs-6 upregulates March1 to suppress bladder cancer growth by sponging miR-653. . 11:11202-11223. https://doi.org/10.18632/aging.102525

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                TY  - JOUR
                AU  - Su, Yinjie 
                AU  - Feng, Weilian 
                AU  - Zhong, Guanglei 
                AU  - Ya, Yiyao 
                AU  - Du, Zehu 
                AU  - Shi, Juanyi 
                AU  - Chen, Luping 
                AU  - Dong, Wen 
                AU  - Lin, Tianxin 
                TI  - ciRs-6 upregulates March1 to suppress bladder cancer growth by sponging miR-653
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102525
                DO  - 10.18632/aging.102525
                SP  - 11202
                EP  - 11223
                PY  - 
                AB  - Background: Circular RNAs have been widely explored as potential biomarkers and therapeutic targets in bladder cancer; however, few have been functionally characterized.Results: ciRs-6 is expressed at low levels in cancer tissues and advanced tumor grades and stages, and its expression correlates with better outcomes for bladder cancer patients. In vitro and in vivo, ciRs-6 was shown to suppress bladder cancer growth by sponging miR-653 to elevate March1 levels. March1 is an E3 ubiquitin ligase that has been proven to suppress bladder cancer growth; knocking down March1 in ciRs-6 overexpressed bladder cancer cells reversed the tumor suppressive effect of ciRs-6.Conclusions: Our study identifies an oncogenic role of ciRs-6 and suggests its usefulness as a novel biomarker for bladder cancer diagnosis and prognosis and as a therapeutic target for bladder cancer.Methods: ciRs-6 was identified by RNA-seq and qPCR; CCK8 assays, clone forming assays and cell cycle analyses were performed to evaluate the in vitro effect of ciRs-6 in bladder cancer; further, a mouse subcutaneous tumor model was designed for in vivo analysis. RNA pulldown assays, miRNA capture experiments and dual luciferase assessments were applied for mechanistic studies.
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Genomic landscapes by multiregion sequencing combined with circulation tumor DNA detection contribute to molecular diagnosis in glioblastomas

Chao Yang, Yanli Tan, Shouwei Li, Junhu Zhou, Qixue Wang, Yunfei Wang, Yingbin Xie, Luyue Chen, Jie Li, Chuan Fang, Chunsheng Kang,

https://doi.org/10.18632/aging.102526 pp 11224—11243

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Yang C, Tan Y, Li S, Zhou J, Wang Q, Wang Y, Xie Y, Chen L, Li J, Fang C, Kang C, . Genomic landscapes by multiregion sequencing combined with circulation tumor DNA detection contribute to molecular diagnosis in glioblastomas. . 11:11224-11243. https://doi.org/10.18632/aging.102526

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                TY  - JOUR
                AU  - Yang, Chao 
                AU  - Tan, Yanli 
                AU  - Li, Shouwei 
                AU  - Zhou, Junhu 
                AU  - Wang, Qixue 
                AU  - Wang, Yunfei 
                AU  - Xie, Yingbin 
                AU  - Chen, Luyue 
                AU  - Li, Jie 
                AU  - Fang, Chuan 
                AU  - Kang, Chunsheng 
                TI  - Genomic landscapes by multiregion sequencing combined with circulation tumor DNA detection contribute to molecular diagnosis in glioblastomas
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102526
                DO  - 10.18632/aging.102526
                SP  - 11224
                EP  - 11243
                PY  - 
                AB  - Glioblastoma is a highly aggressive brain malignancy with a poor prognosis. Its high intratumor heterogeneity contributes to therapeutic resistance, tumor progression and recurrence. We sequenced 31 loci in 11 patients with glioblastoma (including one patient with samples available from the primary and recurrent tumors) to determine the genetic basis and intratumor heterogeneity of glioblastoma. By analyzing the somatic mutations, known driver genes were identified, including EGFR, PTEN and TP53, and the MUC16 gene exhibited the highest mutation rate in the samples examined. Through an evolutionary analysis of the sequencing results, the EGFR p.L861Q mutation was determined to play a role in the progression from the primary tumor to a relapsing tumor in one patient. We analyzed 1403 genes in blood-derived ctDNA that were previously revealed to play a role in tumorigenesis and the progression of cancer. Somatic mutations identified through ctDNA sequencing that match the results of multipoint exon sequencing in tumor tissues were detected, such as EGFR p.L861Q. These findings provide new insights into the intratumor heterogeneity and evolution of glioblastoma. In addition, ctDNA detection in blood samples represents a convenient method to dynamically identify the genetic changes and new therapeutic targets during the treatment of glioblastoma.
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Identification of novel genes associated with longevity in Drosophila melanogaster - a computational approach

Bethany S. Hall, Yvonne A. Barnett, Jonathan J. Crofts, Nadia Chuzhanova,

https://doi.org/10.18632/aging.102527 pp 11244—11267

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Hall BS, Barnett YA, Crofts JJ, Chuzhanova N, . Identification of novel genes associated with longevity in Drosophila melanogaster - a computational approach. . 11:11244-11267. https://doi.org/10.18632/aging.102527

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 TY - JOUR
 AU - Hall, Bethany S. 
 AU - Barnett, Yvonne A. 
 AU - Crofts, Jonathan J. 
 AU - Chuzhanova, Nadia 
 TI - Identification of novel genes associated with longevity in Drosophila melanogaster - a computational approach
 JO - 
 JA - 
 VL - 11
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102527
 DO - 10.18632/aging.102527
 SP - 11244
 EP - 11267
 PY - 
 AB - Despite a growing number of studies on longevity in Drosophila, genetic factors influencing lifespan are still poorly understood. In this paper we propose a conceptually new approach for the identification of novel longevity-associated genes and potential target genes for SNPs in non-coding regions by utilizing the knowledge of co-location of various loci, governed by the three-dimensional architecture of the Drosophila genome. Firstly, we created networks between genes/genomic regions harboring SNPs deemed to be significant in two longevity GWAS summary statistics datasets using intra- and inter-chromosomal interaction frequencies (Hi-C data) as a measure of co-location. These networks were further extended to include regions strongly interacting with previously selected regions. Using various network measures, literature search and additional bioinformatics resources, we investigated the plausibility of genes found to have genuine association with longevity. Several of the newly identified genes were common between the two GWAS datasets and these possessed human orthologs. We also found that the proportion of non-coding SNPs in borders between topologically associated domains is significantly higher than expected by chance. Assuming co-location, we investigated potential target genes for non-coding SNPs. This approach therefore offers a stepping stone to identification of novel genes and SNP targets linked to human longevity.
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The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage

Jaana van Gastel, Hanne Leysen, Paula Santos-Otte, Jhana O. Hendrickx, Abdelkrim Azmi, Bronwen Martin, Stuart Maudsley,

https://doi.org/10.18632/aging.102528 pp 11268—11313

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van Gastel J, Leysen H, Santos-Otte P, Hendrickx JO, Azmi A, Martin B, Maudsley S, . The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage. . 11:11268-11313. https://doi.org/10.18632/aging.102528

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                TY  - JOUR
                AU  - van Gastel, Jaana 
                AU  - Leysen, Hanne 
                AU  - Santos-Otte, Paula 
                AU  - Hendrickx, Jhana O. 
                AU  - Azmi, Abdelkrim 
                AU  - Martin, Bronwen 
                AU  - Maudsley, Stuart 
                TI  - The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102528
                DO  - 10.18632/aging.102528
                SP  - 11268
                EP  - 11313
                PY  - 
                AB  - DNA damage response (DDR) processes, often caused by oxidative stress, are important in aging and -related disorders. We recently showed that G protein-coupled receptor (GPCR) kinase interacting protein 2 (GIT2) plays a key role in both DNA damage and oxidative stress. Multiple tissue analyses in GIT2KO mice demonstrated that GIT2 expression affects the GPCR relaxin family peptide 3 receptor (RXFP3), and is thus a therapeutically-targetable system. RXFP3 and GIT2 play similar roles in metabolic aging processes. Gaining a detailed understanding of the RXFP3-GIT2 functional relationship could aid the development of novel anti-aging therapies. We determined the connection between RXFP3 and GIT2 by investigating the role of RXFP3 in oxidative stress and DDR. Analyzing the effects of oxidizing (H2O2) and DNA-damaging (camptothecin) stressors on the interacting partners of RXFP3 using Affinity Purification-Mass Spectrometry, we found multiple proteins linked to DDR and cell cycle control. RXFP3 expression increased in response to DNA damage, overexpression, and Relaxin 3-mediated stimulation of RXFP3 reduced phosphorylation of DNA damage marker H2AX, and repair protein BRCA1, moderating DNA damage. Our data suggests an RXFP3-GIT2 system that could regulate cellular degradation after DNA damage, and could be a novel mechanism for mitigating the rate of age-related damage accumulation.
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CircPTPRA acts as a tumor suppressor in bladder cancer by sponging miR-636 and upregulating KLF9

Qingqing He, Lifang Huang, Dong Yan, Junming Bi, Meihua Yang, Jian Huang, Tianxin Lin,

https://doi.org/10.18632/aging.102530 pp 11314—11328

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He Q, Huang L, Yan D, Bi J, Yang M, Huang J, Lin T, . CircPTPRA acts as a tumor suppressor in bladder cancer by sponging miR-636 and upregulating KLF9. . 11:11314-11328. https://doi.org/10.18632/aging.102530

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                TY  - JOUR
                AU  - He, Qingqing 
                AU  - Huang, Lifang 
                AU  - Yan, Dong 
                AU  - Bi, Junming 
                AU  - Yang, Meihua 
                AU  - Huang, Jian 
                AU  - Lin, Tianxin 
                TI  - CircPTPRA acts as a tumor suppressor in bladder cancer by sponging miR-636 and upregulating KLF9
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102530
                DO  - 10.18632/aging.102530
                SP  - 11314
                EP  - 11328
                PY  - 
                AB  - Growing evidence suggests that circular RNAs (circRNAs) play pivotal roles in cancer progression. In this study, bioinformatic analysis identified a dysregulated circRNA termed circPTPRA in bladder cancer (BC). By using qRT-PCR analysis, we verified that circPTPRA is down-regulated in clinical BC specimens compared with the matched non-tumor samples, while correlation analyses showed that low circPTPRA expression is associated with poor prognosis, advanced tumor stage and larger tumor size. Based on these findings, we conducted functional assays and revealed that circPTPRA inhibits BC cell proliferation in vitro and tumor growth in vivo. In addition, RNA pull-down, miRNA capture, FISH, and luciferase reporter assays demonstrated that circPTPRA can directly sponge miR-636. Cell transfection experiments showed that miR-636 promotes the proliferation of BC cells by decreasing the expression of Kr&#xFC;ppel Like Factor 9 (KLF9) upon binding to the 3&#x2019;UTR of its mRNA.Further analysis confirmed that circPTPRA competitively sponges miR-636 to upregulate the KLF9 expression, leading to decreased proliferation of BC cells. Our investigation indicates that circPTPRA acts as a tumor suppressor in BC, and suggests that this circRNA may be a novel prognostic biomarker and therapeutic target in BC.
                ER  -

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Interplay of MKP-1 and Nrf2 drives tumor growth and drug resistance in non-small cell lung cancer

Hongyan Wang, Kaihua Liu, Zhexu Chi, Xihang Zhou, Guoping Ren, Ren Zhou, Yinyan Li, Xiuwen Tang, Xiu Jun Wang,

https://doi.org/10.18632/aging.102531 pp 11329—11346

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Wang H, Liu K, Chi Z, Zhou X, Ren G, Zhou R, Li Y, Tang X, Wang XJ, . Interplay of MKP-1 and Nrf2 drives tumor growth and drug resistance in non-small cell lung cancer. . 11:11329-11346. https://doi.org/10.18632/aging.102531

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                TY  - JOUR
                AU  - Wang, Hongyan 
                AU  - Liu, Kaihua 
                AU  - Chi, Zhexu 
                AU  - Zhou, Xihang 
                AU  - Ren, Guoping 
                AU  - Zhou, Ren 
                AU  - Li, Yinyan 
                AU  - Tang, Xiuwen 
                AU  - Wang, Xiu Jun 
                TI  - Interplay of MKP-1 and Nrf2 drives tumor growth and drug resistance in non-small cell lung cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102531
                DO  - 10.18632/aging.102531
                SP  - 11329
                EP  - 11346
                PY  - 
                AB  - Alterations in KEAP1/ NF-E2 p45-related factor 2 (NFE2L2/Nrf2) signaling pathway have been reported in 23% lung adenocarcinoma patients, suggesting that deregulation of the pathway is a major cancer driver. Here we report that mitogen-activated protein (MAP) kinase phosphatase 1 (MKP-1) drives tumor growth and drug resistance by up regulating transcription factor Nrf2. In non-small cell lung cancer (NSCLC) cells and xenografts, MKP-1 knockdown triggered the down-regulation of the metabolic enzymes and cytoprotective proteins, which are the target genes of Nrf2. Consequently, the cell growth was markedly inhibited with decrease of tumor metabolisms and GSH contents. Moreover, MKP-1 silencing sensitized NSCLC cells to cisplatin treatment. Mechanistically, MKP-1 inhibited the ubiquitylation of Nrf2 via a direct interaction with the transcription factor. Nrf2 was hence stabilized and its transcriptional program was activated. Notably, Nrf2 elevated MKP-1 expression at transcriptional level. In human lung adenoma tumor samples, high levels of expression of MKP-1, Nrf2, and its target gene heme oxygenase 1 were closely correlated. Thus, MKP-1 and Nrf2 form a forward feedback loop in lung cancer cells, which stabilizing and activating Nrf2 to promote anabolic metabolism and GSH biosynthesis. This study uncovers a novel role of MKP-1 in the malignant evolution of cancers.
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Risk of ischemic stroke in patients with hypertrophic cardiomyopathy in the absence of atrial fibrillation – a nationwide cohort study

Ting-Tse Lin, Yen-Ling Sung, Tsung-Yu Ko, Chih-Kuo Lee, Lian-Yu Lin, Jimmy Ji-Ming Juang, Cho-Kai Wu,

https://doi.org/10.18632/aging.102532 pp 11347—11357

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Lin T, Sung Y, Ko T, Lee C, Lin L, Juang JJ, Wu C, . Risk of ischemic stroke in patients with hypertrophic cardiomyopathy in the absence of atrial fibrillation – a nationwide cohort study. . 11:11347-11357. https://doi.org/10.18632/aging.102532

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                TY  - JOUR
                AU  - Lin, Ting-Tse 
                AU  - Sung, Yen-Ling 
                AU  - Ko, Tsung-Yu 
                AU  - Lee, Chih-Kuo 
                AU  - Lin, Lian-Yu 
                AU  - Juang, Jimmy Ji-Ming 
                AU  - Wu, Cho-Kai 
                TI  - Risk of ischemic stroke in patients with hypertrophic cardiomyopathy in the absence of atrial fibrillation – a nationwide cohort study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102532
                DO  - 10.18632/aging.102532
                SP  - 11347
                EP  - 11357
                PY  - 
                AB  - Ischemic stroke (IS) is a catastrophic complication of hypertrophic cardiomyopathy (HCM) with aging. We investigated the incidence of IS in HCM patients without atrial fibrillation (AF) and compared the relative risk of IS with matched general population with AF. This study identified 17,371 HCM patients without AF and utilized propensity-score-matching to identify one-to-one matched control of general population with AF receiving oral anti-coagulants (OACs). During a median follow-up of 7.3 years, 847 (4.9%) subjects experienced IS with the incidence of 0.589/100 person-years. The corresponding matched controls experienced 788 (4.5%) events with the incidence of 0.494/100 person-years. Compared with control, HCM patients had similar risk of IS (Hazard ratios [HRs] 0.965, 95% confidence interval [CI] 0.854-1.091). HCM patients with age above 65 years had a significantly increased risk of IS (age 65-74 years, HR 1.278, 95% CI 1.070-1.335; age &#x2265;75 years, HR 1.757, 95% CI 1.435-2.152). Stratified by CHA2DS2-VASc score, HCM subjects with score 0, 1 and 2 had significantly increased risk of IS than control while those with score &#x2265;2 had similar risk as control. Compared with general population with AF, HCM patients without AF had similar risk of IS, suggesting OACs might be necessary in HCM patient without AF.
                ER  -

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LINC00682 inhibits gastric cancer cell progression via targeting microRNA-9-LMX1A signaling axis

Xiaohong Zhang, Jian Li, Fan Li, Zhen Zhao, Li Feng,

https://doi.org/10.18632/aging.102533 pp 11358—11368

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Zhang X, Li J, Li F, Zhao Z, Feng L, . LINC00682 inhibits gastric cancer cell progression via targeting microRNA-9-LMX1A signaling axis. . 11:11358-11368. https://doi.org/10.18632/aging.102533

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Provider: 
 TY - JOUR
 AU - Zhang, Xiaohong 
 AU - Li, Jian 
 AU - Li, Fan 
 AU - Zhao, Zhen 
 AU - Feng, Li 
 TI - LINC00682 inhibits gastric cancer cell progression via targeting microRNA-9-LMX1A signaling axis
 JO - 
 JA - 
 VL - 11
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102533
 DO - 10.18632/aging.102533
 SP - 11358
 EP - 11368
 PY - 
 AB - microRNA-9 (&#x201C;miR-9&#x201D;), upregulated in human gastric cancer (GC) tissues, targets LMX1A (LIM homeobox transcription factor 1&#x3B1;) to promote GC cell progression. The underlying mechanism of miR-9 upregulation in GC is still unknown. Through searching multiple long non-coding RNA (LncRNA) databases, we here discovered that the long non-coding RNA LINC00682 (long intergenic non-protein coding RNA 682) putatively targets miR-9. We show that ectopic overexpression of LINC00682 induced miR-9 downregulation but LMX1A upregulation, inhibiting AGS cell survival, proliferation, migration and invasion. Significant apoptosis activation was detected in LINC00682-overexpressed AGS cells. Contrarily, LINC00682 knockdown induced miR-9 upregulation but LMX1A downregulation, promoting AGS cell survival, proliferation, migration and invasion. In the primary human GC cells, forced LINC00682 overexpression similarly induced miR-9 downregulation and LMX1A upregulation, causing proliferation inhibition and apoptosis activation. Significantly, restoring miR-9 expression by a lentiviral construct reversed LINC00682-induced actions in GC cells. Furthermore, LINC00682 was ineffective in LMX1A KO AGS cells. Importantly, LINC00682 expression levels are significantly downregulated in human GC tissues. We conclude that LINC00682 inhibits GC cell progression via targeting miR-9-LMX1A signaling axis.
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Posttranscriptional regulation of AKT by circular RNA angiomotin- like 1 mediates chemoresistance against paclitaxel in breast cancer cells

Jian Ma, Ling Fang, Qi Yang, Steven Hibberd, William W. Du, Nan Wu, Burton B. Yang,

https://doi.org/10.18632/aging.102535 pp 11369—11381

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Ma J, Fang L, Yang Q, Hibberd S, Du WW, Wu N, Yang BB, . Posttranscriptional regulation of AKT by circular RNA angiomotin- like 1 mediates chemoresistance against paclitaxel in breast cancer cells. . 11:11369-11381. https://doi.org/10.18632/aging.102535

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                TY  - JOUR
                AU  - Ma, Jian 
                AU  - Fang, Ling 
                AU  - Yang, Qi 
                AU  - Hibberd, Steven 
                AU  - Du, William W. 
                AU  - Wu, Nan 
                AU  - Yang, Burton B. 
                TI  - Posttranscriptional regulation of AKT by circular RNA angiomotin- like 1 mediates chemoresistance against paclitaxel in breast cancer cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102535
                DO  - 10.18632/aging.102535
                SP  - 11369
                EP  - 11381
                PY  - 
                AB  - Chemoresistance of triple negative breast cancer against paclitaxel (PAX) is one of the major issues for the patients under chemotherapy. However, the mechanism by which the breast cancer cells are resistant to PAX remains unclear. Here, we identified a circular RNA of angiomotin-like 1 (circAMOTL1) as an important player which may be responsible for the adverse resistance against PAX in breast cancer cells. The circAMOTL1 were overexpressed in MDA-MB-231 breast cancer cells via transfection of circAMOTL1 construct. Overexpression of circAMOTL1 caused significant increase of cell viability, reduction of apoptosis, and enhancement of invasion when MDA-MB-231 cells were exposed to PAX compared to those cells with vector control. Moreover, these resistant effects could be blocked by the application of circAMOTL1 siRNA. In these circAMOTL1 overexpressing cells, we found notable increase of both phosphorylated and total AKT protein, which suggested that AKT might be the downstream factor mediating the resistant effects. Consequently, the gene and protein expression of AKT related pro-apoptotic (BAX and BAK) and anti-apoptotic (BCL-2) factors were significantly changed by circAMOTL1 as well. These results suggest circAMOTL1 may play an important role in the PAX resistance of breast cancer cells via regulation of AKT pathway, facilitation of anti-apoptotic protein and inhibition of pro-apoptotic protein. While providing a new mechanism of PAX resistance in breast cancer cells, our findings may lay groundwork for a novel therapeutic target of the breast cancer treatment in the future.
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Young age at diagnosis is associated with better prognosis in stage IV breast cancer

Wei Liu, Xi-feng Xiong, Yu-zhen Mo, Wei-guang Chen, Mei Li, Rong Liang, Zhi-biao Zhang, Zhi Zhang,

https://doi.org/10.18632/aging.102536 pp 11382—11390

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Liu W, Xiong X, Mo Y, Chen W, Li M, Liang R, Zhang Z, Zhang Z, . Young age at diagnosis is associated with better prognosis in stage IV breast cancer. . 11:11382-11390. https://doi.org/10.18632/aging.102536

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                TY  - JOUR
                AU  - Liu, Wei 
                AU  - Xiong, Xi-feng 
                AU  - Mo, Yu-zhen 
                AU  - Chen, Wei-guang 
                AU  - Li, Mei 
                AU  - Liang, Rong 
                AU  - Zhang, Zhi-biao 
                AU  - Zhang, Zhi 
                TI  - Young age at diagnosis is associated with better prognosis in stage IV breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102536
                DO  - 10.18632/aging.102536
                SP  - 11382
                EP  - 11390
                PY  - 
                AB  - Numerous studies have shown that young age is a risk factor in early breast cancer. But for stage IV breast cancer, it is unclear whether age has a similar effect on patient survival. We collected and analyzed data from patients with stage IV breast cancer between January 2010 and December 2015 in SEER database. Multivariate Cox proportional hazard model was used in this study. 13,069 patients with stage IV breast cancer were included in the analysis, of which 1,135 were young breast cancer patients (&#x2264;40 years old). In a multivariate analysis that adjusted for sociodemographic factors, clinical-pathological characteristics and therapeutic methods, the risk of death in patients with stage IV &#x2264;40 years was significantly reduced (hazard ratio [HR], 0.72; 95% CI, 0.65-0.79). Subgroup analyses showed that, with the same adjustment of all factors, young age only significantly reduced the risk of death in patients with luminal A (HR, 0.78; 95% CI, 0.68-0.89) and luminal B (HR 0.46; 95% CI, 0.35-0.60) subtypes. Young age at diagnosis is associated with better survival in patients with stage IV breast cancer. The effect of young age at diagnosis on the survival outcome of stage IV breast cancer varies by subtypes.
                ER  -

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Melatonin protects blood-brain barrier integrity and permeability by inhibiting matrix metalloproteinase-9 via the NOTCH3/NF-κB pathway

Weiwei Qin, Jing Li, Rongjia Zhu, Suhua Gao, Junfen Fan, Mingrong Xia, Robert Chunhua Zhao, Jiewen Zhang,

https://doi.org/10.18632/aging.102537 pp 11391—11415

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Qin W, Li J, Zhu R, Gao S, Fan J, Xia M, Zhao RC, Zhang J, . Melatonin protects blood-brain barrier integrity and permeability by inhibiting matrix metalloproteinase-9 via the NOTCH3/NF-κB pathway. . 11:11391-11415. https://doi.org/10.18632/aging.102537

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                TY  - JOUR
                AU  - Qin, Weiwei 
                AU  - Li, Jing 
                AU  - Zhu, Rongjia 
                AU  - Gao, Suhua 
                AU  - Fan, Junfen 
                AU  - Xia, Mingrong 
                AU  - Zhao, Robert Chunhua 
                AU  - Zhang, Jiewen 
                TI  - Melatonin protects blood-brain barrier integrity and permeability by inhibiting matrix metalloproteinase-9 via the NOTCH3/NF-κB pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102537
                DO  - 10.18632/aging.102537
                SP  - 11391
                EP  - 11415
                PY  - 
                AB  - The pathophysiological mechanism of white matter hyperintensities of cerebral small vessel disease (CSVD) includes an impaired blood-brain barrier (BBB) with increased permeability. Neuroinflammation likely contributes to the disruption of the BBB in CSVD. Therefore, understanding the molecular mechanism of how neuroinflammation causes BBB damage is essential to preventing BBB disruption in CSVD. Matrix metalloproteinase 9 (MMP-9) contributes to BBB damage in neuroinflammatory diseases. In this study, we observed that interleukin-1&#x3B2; (IL-1&#x3B2;)-induced MMP-9 secretion in pericytes increased BBB permeability to sodium fluorescein (Na-F) by damaging the disruption of VE-cadherin, occludin, claudin-5, and zonula occludin-1 (ZO-1). Melatonin reduced BBB permeability to Na-F and inhibited the disruption of the adherens and tight junction proteins. Melatonin also downregulated MMP-9 and upregulated tissue inhibitor of metalloproteinases 1 (TIMP-1) gene expression, which decreased the MMP-9/TIMP-1 ratio. In addition, nuclear translocation of NF-&#x3BA;B/p65 induced by IL-1&#x3B2; in pericytes upregulated MMP-9 expression, which was inhibited by the NF-&#x3BA;B inhibitor PDTC. However, the NOTCH3 inhibitor DAPT significantly inhibited NF-&#x3BA;B/p65 translocation to the nucleus, while melatonin in combination with DAPT significantly prevented NF-&#x3BA;B/p65 translocation than DAPT alone. Our results suggest that melatonin reduced MMP-9-induced permeability of the BBB. Melatonin reduced MMP-9 expression and activity, which was induced by IL-1&#x3B2; through the regulation of the NOTCH3/NF-&#x3BA;B signaling pathway in pericytes, suggesting that pericytes regulate BBB integrity and function.
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Dysregulation of pseudogene/lncRNA-hsa-miR-363-3p-SPOCK2 pathway fuels stage progression of ovarian cancer

Weiyang Lou, Bisha Ding, Guansheng Zhong, Chengyong Du, Weimin Fan, Peifen Fu,

https://doi.org/10.18632/aging.102538 pp 11416—11439

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Lou W, Ding B, Zhong G, Du C, Fan W, Fu P, . Dysregulation of pseudogene/lncRNA-hsa-miR-363-3p-SPOCK2 pathway fuels stage progression of ovarian cancer. . 11:11416-11439. https://doi.org/10.18632/aging.102538

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                TY  - JOUR
                AU  - Lou, Weiyang 
                AU  - Ding, Bisha 
                AU  - Zhong, Guansheng 
                AU  - Du, Chengyong 
                AU  - Fan, Weimin 
                AU  - Fu, Peifen 
                TI  - Dysregulation of pseudogene/lncRNA-hsa-miR-363-3p-SPOCK2 pathway fuels stage progression of ovarian cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102538
                DO  - 10.18632/aging.102538
                SP  - 11416
                EP  - 11439
                PY  - 
                AB  - Objective: Ovarian cancer is one of the most common and lethal cancer types in women. The molecular mechanism of ovarian cancer progression is still unclear.Results: Here, we first reported that expression levels of three genes, GJB2, S100A2 and SPOCK2, were significantly higher in advanced stage than that in early stage of ovarian cancer, and upregulation of them indicated poor prognosis of patients with ovarian cancer. Subsequently, 8, 6 and 20 miRNAs were predicted to target GJB2, S100A2 and SPOCK2, respectively. Among these miRNA-mRNA pairs, hsa-miR-363-3p-SPOCK2 axis was the most potential in suppressing progression of ovarian cancer. Mechanistically, we found that hsa-miR-363-3p-SPOCK2 axis was involved in regulation of actin cytoskeleton. Moreover, 6 pseudogenes and 8 lncRNAs were identified to potentially inhibit hsa-miR-363-3p-SPOCK2 axis in ovarian cancer.Conclusions: Collectively, we elucidate a regulatory role of pseudogene/lncRNA-hsa-miR-363-3p-SPOCK2 pathway in progression of ovarian cancer, which may provide effective therapeutic approaches and promising prognostic biomarkers for ovarian cancer.Materials and methods: Differentially expressed genes (DEGs) in ovarian cancer were first screened using GSE12470, after which DEGs expression were validated using GEPIA. Kaplan-Meier analysis was employed to assess the prognostic values. Potential miRNAs were predicted by seven target prediction databases, and upstream lncRNAs and pseudogenes of hsa-miR-363-3p were forecasted through miRNet or starBase. UALCAN and starBase were used to obtain the co-expressed genes of SPOCK. Enrichment analysis for these co-expressed genes was performed by Enrichr.
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Prognostic implications of autophagy-associated gene signatures in non-small cell lung cancer

Yang Liu, Ligao Wu, Haijiao Ao, Meng Zhao, Xue Leng, Mingdong Liu, Jianqun Ma, Jinhong Zhu,

https://doi.org/10.18632/aging.102544 pp 11440—11462

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Liu Y, Wu L, Ao H, Zhao M, Leng X, Liu M, Ma J, Zhu J, . Prognostic implications of autophagy-associated gene signatures in non-small cell lung cancer. . 11:11440-11462. https://doi.org/10.18632/aging.102544

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                TY  - JOUR
                AU  - Liu, Yang 
                AU  - Wu, Ligao 
                AU  - Ao, Haijiao 
                AU  - Zhao, Meng 
                AU  - Leng, Xue 
                AU  - Liu, Mingdong 
                AU  - Ma, Jianqun 
                AU  - Zhu, Jinhong 
                TI  - Prognostic implications of autophagy-associated gene signatures in non-small cell lung cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102544
                DO  - 10.18632/aging.102544
                SP  - 11440
                EP  - 11462
                PY  - 
                AB  - Autophagy, a highly conserved cellular proteolysis process, has been involved in non-small cell lung cancer (NSCLC). We tried to develop a prognostic prediction model for NSCLC patients based on the expression profiles of autophagy-associated genes. Univariate Cox regression analysis was used to determine autophagy-associated genes significantly correlated with overall survival (OS) of the TCGA lung cancer cohort. LASSO regression was performed to build multiple-gene prognostic signatures. We found that the 22-gene and 11-gene signatures could dichotomize patients with significantly different OS and independently predict the OS in TCGA lung adenocarcinoma (HR=2.801, 95% CI=2.252-3.486, P&lt;0.001) and squamous cell carcinoma (HR=1.105, 95% CI=1.067-1.145, P&lt;0.001), respectively. The prognostic performance of the 22-gene signature was validated in four GEO lung cancer cohorts. Moreover, GO, KEGG, and GSEA analyses unveiled several fundamental signaling pathways and cellular processes associated with the 22-gene signature in lung adenocarcinoma. We also constructed a clinical nomogram with a concordance index of 0.71 to predict the survival possibility of NSCLC patients by integrating clinical characteristics and the autophagy gene signature. The calibration curves substantiated fine concordance between nomogram prediction and actual observation. Overall, we constructed and verified a novel autophagy-associated gene signature that could improve the individualized outcome prediction in NSCLC.
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LncRNA EPIC1 downregulation mediates hydrogen peroxide-induced neuronal cell injury

Jian Sun, Jinyu Zheng, Ya Li, Ming Yan, Ping Li, Lili Ma,

https://doi.org/10.18632/aging.102545 pp 11463—11473

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Sun J, Zheng J, Li Y, Yan M, Li P, Ma L, . LncRNA EPIC1 downregulation mediates hydrogen peroxide-induced neuronal cell injury. . 11:11463-11473. https://doi.org/10.18632/aging.102545

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                TY  - JOUR
                AU  - Sun, Jian 
                AU  - Zheng, Jinyu 
                AU  - Li, Ya 
                AU  - Yan, Ming 
                AU  - Li, Ping 
                AU  - Ma, Lili 
                TI  - LncRNA EPIC1 downregulation mediates hydrogen peroxide-induced neuronal cell injury
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102545
                DO  - 10.18632/aging.102545
                SP  - 11463
                EP  - 11473
                PY  - 
                AB  - Excessive oxidative stress causes neuronal cell injury. Long non-coding RNA (LncRNA) EPIC1 (Lnc-EPIC1) is a MYC-interacting LncRNA. Its expression and potential functions in hydrogen peroxide (H2O2)-stimulated neuronal cells are studied. In SH-SY5Y neuronal cells and primary human neuron cultures, H2O2 downregulated Lnc-EPIC1 and key MYC targets (Cyclin A1, CDC20 and CDC45). Ectopic overexpression of Lnc-EPIC1 increased expression of MYC targets and significantly attenuated H2O2-induced neuronal cell death and apoptosis. Contrarily, Lnc-EPIC1 siRNA potentiated neuronal cell death by H2O2. MYC knockout by CRISPR/Cas9 method also facilitated H2O2-induced SH-SY5Y cell death. Significantly, MYC knockout abolished Lnc-EPIC1-induced actions in H2O2-stimulated neuronal cells. Together, these results suggest that Lnc-EPIC1 downregulation mediates H2O2-induced neuronal cell death.
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Prognostic value of immune-related genes in clear cell renal cell carcinoma

Bangbei Wan, Bo Liu, Yuan Huang, Gang Yu, Cai Lv,

https://doi.org/10.18632/aging.102548 pp 11474—11489

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Wan B, Liu B, Huang Y, Yu G, Lv C, . Prognostic value of immune-related genes in clear cell renal cell carcinoma. . 11:11474-11489. https://doi.org/10.18632/aging.102548

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                TY  - JOUR
                AU  - Wan, Bangbei 
                AU  - Liu, Bo 
                AU  - Huang, Yuan 
                AU  - Yu, Gang 
                AU  - Lv, Cai 
                TI  - Prognostic value of immune-related genes in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102548
                DO  - 10.18632/aging.102548
                SP  - 11474
                EP  - 11489
                PY  - 
                AB  - Clear cell renal cell carcinoma (ccRCC) is the most common pathological subtype of renal cell carcinoma, and immune-related genes (IRGs) are key contributors to its development. In this study, the gene expression profiles and clinical data of ccRCC patients were downloaded from The Cancer Genome Atlas database and the cBioPortal database, respectively. IRGs were obtained from the ImmPort database. We analyzed the expression of IRGs in ccRCC, and discovered 681 that were differentially expressed between ccRCC and normal kidney tissues. Univariate Cox regression analysis was used to identify prognostic differentially expressed IRGs (PDEIRGs). Using Lasso regression and multivariate Cox regression analyses, we detected seven optimal PDEIRGs (PLAU, ISG15, IRF9, ARG2, RNASE2, SEMA3G and UCN) and used them to construct a risk model to predict the prognosis of ccRCC patients. This model accurately stratified patients with different survival outcomes and precisely identified patients with different mutation burdens. Our findings suggest the seven PDEIRGs identified in this study are valuable prognostic predictors in ccRCC patients. These genes could be used to investigate the developmental mechanisms of ccRCC and to design individualized treatments for ccRCC patients.
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Conditional disease-free survival in high-risk renal cell carcinoma treated with sunitinib

Ning Shao, Hengchuan Su, Dingwei Ye,

https://doi.org/10.18632/aging.102549 pp 11490—11503

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Shao N, Su H, Ye D, . Conditional disease-free survival in high-risk renal cell carcinoma treated with sunitinib. . 11:11490-11503. https://doi.org/10.18632/aging.102549

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                TY  - JOUR
                AU  - Shao, Ning 
                AU  - Su, Hengchuan 
                AU  - Ye, Dingwei 
                TI  - Conditional disease-free survival in high-risk renal cell carcinoma treated with sunitinib
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102549
                DO  - 10.18632/aging.102549
                SP  - 11490
                EP  - 11503
                PY  - 
                AB  - Background: Disease-free survival (DFS) did not reflect accurate individual prognosis after initial diagnosis. As conditional DFS (CDFS) could provide dynamic prognostic information, we evaluated CDFS in these patients treated with or without sunitinib.Results: A total of 1329 patients with median follow-up 6.54 years were enrolled. CDFS improved continuously with disease-free survivorship increasing in both sunitinib and placebo group with minimal difference. In placebo arm, the CDFS of surviving to five year after living 1, 2, 3, and 4 years were 65%, 78%, 87%, and 95% (observed 5-year DFS: 51%). Dynamic changes of HR showed adjuvant sunitinib decrease relapse risks during the first 1.5 years after surgery (P &lt; 0.03).Conclusions: Our study provided contemporary data of CDFS and change of relapse HR in high-risk ccRCC patients after adjuvant sunitinib or placebo. The remarkable improvement in CDFS highlighted the importance of disease-free interval as a strong indicator in patient counseling and surveillance planning.Materials and Methods: The primary end point was CDFS and the second end point was smooth hazard ratios (HR) for the prediction of relapses. The differences of conditional survival were compared with the calculation of d value.
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Resveratrol delays postovulatory aging of mouse oocytes through activating mitophagy

Jilong Zhou, Zhouyiyuan Xue, Hai-Nan He, Xin Liu, Shu-Yuan Yin, Dan-Ya Wu, Xia Zhang, Heide Schatten, Yi-Liang Miao,

https://doi.org/10.18632/aging.102551 pp 11504—11519

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Zhou J, Xue Z, He H, Liu X, Yin S, Wu D, Zhang X, Schatten H, Miao Y, . Resveratrol delays postovulatory aging of mouse oocytes through activating mitophagy. . 11:11504-11519. https://doi.org/10.18632/aging.102551

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                TY  - JOUR
                AU  - Zhou, Jilong 
                AU  - Xue, Zhouyiyuan 
                AU  - He, Hai-Nan 
                AU  - Liu, Xin 
                AU  - Yin, Shu-Yuan 
                AU  - Wu, Dan-Ya 
                AU  - Zhang, Xia 
                AU  - Schatten, Heide 
                AU  - Miao, Yi-Liang 
                TI  - Resveratrol delays postovulatory aging of mouse oocytes through activating mitophagy
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102551
                DO  - 10.18632/aging.102551
                SP  - 11504
                EP  - 11519
                PY  - 
                AB  - Resveratrol (3,5,4&#x2032;-trihydroxystilbene, RSV) is a natural potential anti-aging polyphenolic compound frequently used as a nutritional supplement against several diseases. However, the underlying mechanisms by which resveratrol regulates postovulatory aging of oocytes are still insufficiently known. In this study, we found that resveratrol could delay postovulatory aging and improve developmental competence of oocytes through activating selective mitophagy in the mouse. Resveratrol could maintain spindle morphology but it disturbed cortical granule (CG) distribution during oocyte aging. This might be due to upregulated mitophagy, since blocking mitophagy by cyclosporin A (CsA) treatment affected oocyte quality by damaging mitochondrial function and it decreased embryonic development. In addition, we also observed an involvement of FoxO3a in regulating mitophagy in aging oocytes following resveratrol treatment. Taken together, our results provide evidence that mitophagy induced by resveratrol is a potential mechanism to protect against postovulatory oocyte aging.
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Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes

Qi Peng, Bin Chen, Hao Wang, Ying Zhu, Jinghong Wu, Yetao Luo, Guowei Zuo, Jinyong Luo, Lan Zhou, Qiong Shi, Yaguang Weng, Ailong Huang, Tong-Chuan He, Jiaming Fan,

https://doi.org/10.18632/aging.102552 pp 11520—11540

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Peng Q, Chen B, Wang H, Zhu Y, Wu J, Luo Y, Zuo G, Luo J, Zhou L, Shi Q, Weng Y, Huang A, He T, et al, . Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes. . 11:11520-11540. https://doi.org/10.18632/aging.102552

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                TY  - JOUR
                AU  - Peng, Qi 
                AU  - Chen, Bin 
                AU  - Wang, Hao 
                AU  - Zhu, Ying 
                AU  - Wu, Jinghong 
                AU  - Luo, Yetao 
                AU  - Zuo, Guowei 
                AU  - Luo, Jinyong 
                AU  - Zhou, Lan 
                AU  - Shi, Qiong 
                AU  - Weng, Yaguang 
                AU  - Huang, Ailong 
                AU  - He, Tong-Chuan 
                AU  - Fan, Jiaming 
                TI  - Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102552
                DO  - 10.18632/aging.102552
                SP  - 11520
                EP  - 11540
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Peng, Qi 
                AU  - Chen, Bin 
                AU  - Wang, Hao 
                AU  - Zhu, Ying 
                AU  - Wu, Jinghong 
                AU  - Luo, Yetao 
                AU  - Zuo, Guowei 
                AU  - Luo, Jinyong 
                AU  - Zhou, Lan 
                AU  - Shi, Qiong 
                AU  - Weng, Yaguang 
                AU  - Huang, Ailong 
                AU  - He, Tong-Chuan 
                AU  - Fan, Jiaming 
                TI  - Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102552
                DO  - 10.18632/aging.102552
                SP  - 11520
                EP  - 11540
                PY  - 
                AB  - Liver has numerous critical metabolic functions including lipid metabolism, which is usually dysregulated in obesity, the metabolic syndrome, and non-alcoholic fatty liver disease (NAFLD). Increasing evidence indicates bone morphogenetic proteins (BMPs) play an important role in adipogenesis and thermogenic balance in adipogenic progenitors and adipose tissue. However, the direct impact of BMPs on hepatic steatosis and possible association with NAFLD are poorly understood. Here, we found that BMP4 was up-regulated in oleic acid-induced steatosis and during the development of high fat diet (HFD)-induced NAFLD. Exogenous BMP4 reduced lipid accumulation and up-regulated the genes involved in lipid synthesis, storage and breakdown in hepatocytes. Exogenous BMP4 inhibited hepatic steatosis, reduced serum triglyceride levels and body weight, and alleviated progression of NAFLD in vivo. Mechanistically, BMP4 overexpression in hepatocytes down-regulated most components of the mTORC1 signaling axis. Collectively, these findings strongly suggest that BMP4 may play an essential role in regulating hepatic lipid metabolism and the molecular pathogenesis of NAFLD. Manipulating BMP4 and/or mTORC1 signaling axis may lead to the development of novel therapeutics for obesity, metabolic syndrome, and NAFLD.
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The local translation of K_Na in dendritic projections of auditory neurons and the roles of K_Na in the transition from hidden to overt hearing loss

Jeong Han Lee, Mincheol Kang, Seojin Park, Maria C. Perez-Flores, Xiao-Dong Zhang, Wenying Wang, Michael Anne Gratton, Nipavan Chiamvimonvat, Ebenezer N. Yamoah,

https://doi.org/10.18632/aging.102553 pp 11541—11564

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Lee JH, Kang M, Park S, Perez-Flores MC, Zhang X, Wang W, Gratton MA, Chiamvimonvat N, Yamoah EN, . The local translation of K_Na in dendritic projections of auditory neurons and the roles of K_Na in the transition from hidden to overt hearing loss. . 11:11541-11564. https://doi.org/10.18632/aging.102553

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Provider: 
 TY - JOUR
 AU - Lee, Jeong Han 
 AU - Kang, Mincheol 
 AU - Park, Seojin 
 AU - Perez-Flores, Maria C. 
 AU - Zhang, Xiao-Dong 
 AU - Wang, Wenying 
 AU - Gratton, Michael Anne 
 AU - Chiamvimonvat, Nipavan 
 AU - Yamoah, Ebenezer N. 
 TI - The local translation of KNa in dendritic projections of auditory neurons and the roles of KNa in the transition from hidden to overt hearing loss
 JO - 
 JA - 
 VL - 11
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102553
 DO - 10.18632/aging.102553
 SP - 11541
 EP - 11564
 PY - 
 AB - Local and privileged expression of dendritic proteins allows segregation of distinct functions in a single neuron but may represent one of the underlying mechanisms for early and insidious presentation of sensory neuropathy. Tangible characteristics of early hearing loss (HL) are defined in correlation with nascent hidden hearing loss (HHL) in humans and animal models. Despite the plethora of causes of HL, only two prevailing mechanisms for HHL have been identified, and in both cases, common structural deficits are implicated in inner hair cell synapses, and demyelination of the auditory nerve (AN). We uncovered that Na+-activated K+ (KNa) mRNA and channel proteins are distinctly and locally expressed in dendritic projections of primary ANs and genetic deletion of KNa channels (Kcnt1 and Kcnt2) results in the loss of proper AN synaptic function, characterized as HHL, without structural synaptic alterations. We further demonstrate that the local functional synaptic alterations transition from HHL to increased hearing-threshold, which entails changes in global Ca2+ homeostasis, activation of caspases 3/9, impaired regulation of inositol triphosphate receptor 1 (IP3R1), and apoptosis-mediated neurodegeneration. Thus, the present study demonstrates how local synaptic dysfunction results in an apparent latent pathological phenotype (HHL) and, if undetected, can lead to overt HL. It also highlights, for the first time, that HHL can precede structural synaptic dysfunction and AN demyelination. The stepwise cellular mechanisms from HHL to canonical HL are revealed, providing a platform for intervention to prevent lasting and irreversible age-related hearing loss (ARHL).
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Nrf2 activation mediates tumor-specific hepatic stellate cells-induced DIgR2 expression in dendritic cells

Yun-Hong Xia, Zhen Lu, Shou-Min Wang, Li-Xia Hu,

https://doi.org/10.18632/aging.102554 pp 11565—11575

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Xia Y, Lu Z, Wang S, Hu L, . Nrf2 activation mediates tumor-specific hepatic stellate cells-induced DIgR2 expression in dendritic cells. . 11:11565-11575. https://doi.org/10.18632/aging.102554

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                TY  - JOUR
                AU  - Xia, Yun-Hong 
                AU  - Lu, Zhen 
                AU  - Wang, Shou-Min 
                AU  - Hu, Li-Xia 
                TI  - Nrf2 activation mediates tumor-specific hepatic stellate cells-induced DIgR2 expression in dendritic cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102554
                DO  - 10.18632/aging.102554
                SP  - 11565
                EP  - 11575
                PY  - 
                AB  - Our previous studies discovered that tumor-specific hepatic stellate cells (tHSCs) induced dendritic cell-derived immunoglobulin receptor 2 (DIgR2) expression in bone marrow-derived dendritic cells (mDCs), inhibiting splenic T cell activation. The current study aims to explore the underlying mechanism of DIgR2 expression by focusing on Nrf2 (nuclear-factor-E2-related factor 2) signaling. We show that tHSCs co-culture induced significant Nrf2 signaling activation in mDCs. The latter was evidenced by Nrf2-Keap1 disassociation, Nrf2 protein stabilization, accumulation and nuclear translocation. Expression of Nrf2-dependent genes, including heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1), were detected in tHSCs-co-cultured mDCs. Importantly tHSCs-induced DIgR2 expression was blocked by Nrf2 shRNA or knockout (KO, by CRISPR/Cas9 method). Conversely, forced activation of Nrf2, by Keap1 shRNA or the Nrf2 activators (3H-1,2-dithiole-3-thione and MIND4-17), induced significant DIgR2 expression. tHSCs stimulation induced reactive oxygen species (ROS) production in mDCs. Conversely, ROS scavengers inhibited tHSCs-induced ROS production, Nrf2 activation and DIgR2 expression in mDCs. Significantly, tHSCs inhibited production of multiple cytokines (CD80, CD86 and IL-12) in mDCs, reversed by Nrf2 depletion. Moreover, Nrf2 shRNA or KO attenuated splenic T cell inhibition by tHSCs-stimulated mDCs. Together, we conclude that Nrf2 activation mediates tHSCs-induced DIgR2 expression in mDCs.
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Robust immunoscore model to predict the response to anti-PD1 therapy in melanoma

Run-Cong Nie, Shu-Qiang Yuan, Yun Wang, Ying-Bo Chen, Yan-Yu Cai, Shi Chen, Shu-Man Li, Jie Zhou, Guo-Ming Chen, Tian-Qi Luo, Zhi-Wei Zhou, Yuan-Fang Li,

https://doi.org/10.18632/aging.102556 pp 11576—11590

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Nie R, Yuan S, Wang Y, Chen Y, Cai Y, Chen S, Li S, Zhou J, Chen G, Luo T, Zhou Z, Li Y, . Robust immunoscore model to predict the response to anti-PD1 therapy in melanoma. . 11:11576-11590. https://doi.org/10.18632/aging.102556

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                TY  - JOUR
                AU  - Nie, Run-Cong 
                AU  - Yuan, Shu-Qiang 
                AU  - Wang, Yun 
                AU  - Chen, Ying-Bo 
                AU  - Cai, Yan-Yu 
                AU  - Chen, Shi 
                AU  - Li, Shu-Man 
                AU  - Zhou, Jie 
                AU  - Chen, Guo-Ming 
                AU  - Luo, Tian-Qi 
                AU  - Zhou, Zhi-Wei 
                AU  - Li, Yuan-Fang 
                TI  - Robust immunoscore model to predict the response to anti-PD1 therapy in melanoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102556
                DO  - 10.18632/aging.102556
                SP  - 11576
                EP  - 11590
                PY  - 
                AB  - This study aimed to construct immune-related predictors to identify responders to anti-PD1 therapy of melanoma through CIBERSORT algorithm. Using the least absolute shrinkage and selection operator (LASSO) logistic regression, we constructed an immunoscore consisting of 8 immune subsets to predict the anti-PD1 response. This score achieved an overall accuracy of AUC = 0.77, 0.80 and 0.73 in the training cohort, validation cohort and on-anti-PD1 cohort, respectively. Patients with high immunoscores had significantly higher objective response rates (ORRs) than did those with low immunoscores (ORR: 53.8% vs 17.7%, P &lt; 0.001 for entire pre-anti-PD1 cohort; 42.1% vs 15.1%, P = 0.022 for on-anti-PD1 cohort; 66.7% vs 16.7%, P = 0.038 for neoadjuvant anti-PD1 cohort). Prolonged survival trends were observed in high-immunoscore group (1-year PFS: 42.4% vs 14.3%, P = 0.059; 3-year OS: 41.5% vs 31.6%, P = 0.057). Furthermore, we found that high-immunoscore group exhibited higher fractions of tumor-infiltrating lymphocytes and an increased IFN-&#x3B3; response. Analysis of the results of the GSEA indicated a significant enrichment of antitumor immunity pathways in the high-immunoscore group. Therefore, this study indicated that we constructed a robust immunoscore model to predict the anti-PD1 response of metastatic melanoma and the neoadjuvant anti-PD1 response of resectable melanoma.
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Pharmacological inhibition of G9a/GLP restores cognition and reduces oxidative stress, neuroinflammation and β-Amyloid plaques in an early-onset Alzheimer’s disease mouse model

Christian Griñán-Ferré, Laura Marsal-García, Aina Bellver-Sanchis, Shukkoor Muhammed Kondengaden, Ravi Chakra Turga, Santiago Vázquez, Mercè Pallàs,

https://doi.org/10.18632/aging.102558 pp 11591—11608

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Griñán-Ferré C, Marsal-García L, Bellver-Sanchis A, Kondengaden SM, Turga RC, Vázquez S, Pallàs M, . Pharmacological inhibition of G9a/GLP restores cognition and reduces oxidative stress, neuroinflammation and β-Amyloid plaques in an early-onset Alzheimer’s disease mouse model. . 11:11591-11608. https://doi.org/10.18632/aging.102558

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                TY  - JOUR
                AU  - Griñán-Ferré, Christian 
                AU  - Marsal-García, Laura 
                AU  - Bellver-Sanchis, Aina 
                AU  - Kondengaden, Shukkoor Muhammed 
                AU  - Turga, Ravi Chakra 
                AU  - Vázquez, Santiago 
                AU  - Pallàs, Mercè 
                TI  - Pharmacological inhibition of G9a/GLP restores cognition and reduces oxidative stress, neuroinflammation and β-Amyloid plaques in an early-onset Alzheimer’s disease mouse model
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102558
                DO  - 10.18632/aging.102558
                SP  - 11591
                EP  - 11608
                PY  - 
                AB  - The implication of epigenetic mechanisms in Alzheimer&#x2019;s disease (AD) has been demonstrated in several studies. UNC0642, a specific and potent inhibitor of methyltransferase activity G9a/GLP (G9a-like) complex, was evaluated in the 5XFAD mouse model. UNC0642 treatment rescued 5XFAD cognition impairment, reduced DNA-methylation (5-mC), increased hydroxymethylation (5-hmC), and decreased the di-methylation of lysine 9 of histone H3 (H3K9me2) levels in the hippocampus. Increases in the Nuclear Factor erythroid-2-Related Factor 2 (NRF2), Heme oxygenase decycling 1 (Hmox1) gene expression, and diminution in Reactive Oxygen Species (ROS) were also reported. Moreover, neuroinflammatory markers, such as Interleukin 6 (Il-6), Tumor necrosis factor-alpha (Tnf-&#x3B1;) gene expression, and Glial fibrillary acidic protein (GFAP) immunofluorescence were reduced by UNC0642 treatment. An increase in Nerve growth factor (Ngf), Nerve growth factor inducible (Vgf) gene expression, Brain-derived neurotrophic factor (BDNF), and Synaptophysin (SYN) were found after UNC0642 treatment. Importantly, a reduction in &#x3B2;-amyloid plaques was also observed. In conclusion, our work demonstrates that the inhibition of the G9a/GLP complex by UNC0642 delivered significant neuroprotective effects in 5XFAD mice, point out G9a/GLP as a new target for AD.
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Long noncoding RNA NR2F1-AS1 enhances the malignant properties of osteosarcoma by increasing forkhead box A1 expression via sponging of microRNA-483-3p

Shenglong Li, Ke Zheng, Yi Pei, Wei Wang, Xiaojing Zhang,

https://doi.org/10.18632/aging.102563 pp 11609—11623

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Li S, Zheng K, Pei Y, Wang W, Zhang X, . Long noncoding RNA NR2F1-AS1 enhances the malignant properties of osteosarcoma by increasing forkhead box A1 expression via sponging of microRNA-483-3p. . 11:11609-11623. https://doi.org/10.18632/aging.102563

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 TY - JOUR
 AU - Li, Shenglong 
 AU - Zheng, Ke 
 AU - Pei, Yi 
 AU - Wang, Wei 
 AU - Zhang, Xiaojing 
 TI - Long noncoding RNA NR2F1-AS1 enhances the malignant properties of osteosarcoma by increasing forkhead box A1 expression via sponging of microRNA-483-3p
 JO - 
 JA - 
 VL - 11
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102563
 DO - 10.18632/aging.102563
 SP - 11609
 EP - 11623
 PY - 
 AB - The long noncoding RNA NR2F1-AS1 has been found to promote the development of hepatocellular carcinoma and endometrial cancer. In this study, we measured NR2F1-AS1 expression in osteosarcoma (OS), determined the involvement of NR2F1-AS1 in the malignant properties of OS, and investigated the underlying mechanisms. NR2F1-AS1 was found to be upregulated in OS tumors and cell lines. The increased NR2F1-AS1 level was closely associated with advanced clinical stage and distant metastasis in patients with OS. Patients with OS in an NR2F1-AS1 high-expression group demonstrated significantly shorter overall survival than did patients in an NR2F1-AS1 low-expression group. NR2F1-AS1 knockdown inhibited OS cell proliferation, migration, and invasion and promoted cell cycle arrest and apoptosis in vitro and slowed tumor growth in vivo. NR2F1-AS1 was found to function as a competing endogenous RNA by directly sponging microRNA-483-3p (miR-483-3p) and upregulating its target oncogene forkhead box A1 (FOXA1). Finally, rescue experiments revealed that knockdown of miR-483-3p and recovery of FOXA1 expression both attenuated the influence of the NR2F1-AS1 knockdown on OS cells. Thus, NR2F1-AS1 plays an oncogenic role in OS through sponging miR-483-3p and thereby upregulating FOXA1, suggesting an additional target for osteosarcoma therapeutics.
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Stimulation of MMP-9 of oral epithelial cells by areca nut extract is related to TGF-β/Smad2-dependent and –independent pathways and prevented by betel leaf extract, hydroxychavicol and melatonin

Mei-Chi Chang, Yu-Hwa Pan, Hsyueh-Liang Wu, Yi-Jie Lu, Wan-Chuen Liao, Chien-Yang Yeh, Jang-Jaer Lee, Jiiang-Huei Jeng,

https://doi.org/10.18632/aging.102565 pp 11624—11639

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Chang M, Pan Y, Wu H, Lu Y, Liao W, Yeh C, Lee J, Jeng J, . Stimulation of MMP-9 of oral epithelial cells by areca nut extract is related to TGF-β/Smad2-dependent and –independent pathways and prevented by betel leaf extract, hydroxychavicol and melatonin. . 11:11624-11639. https://doi.org/10.18632/aging.102565

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                TY  - JOUR
                AU  - Chang, Mei-Chi 
                AU  - Pan, Yu-Hwa 
                AU  - Wu, Hsyueh-Liang 
                AU  - Lu, Yi-Jie 
                AU  - Liao, Wan-Chuen 
                AU  - Yeh, Chien-Yang 
                AU  - Lee, Jang-Jaer 
                AU  - Jeng, Jiiang-Huei 
                TI  - Stimulation of MMP-9 of oral epithelial cells by areca nut extract is related to TGF-β/Smad2-dependent and –independent pathways and prevented by betel leaf extract, hydroxychavicol and melatonin
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102565
                DO  - 10.18632/aging.102565
                SP  - 11624
                EP  - 11639
                PY  - 
                AB  - Background: There are 200-600 million betel quid (BQ) chewers in the world. BQ increases oral cancer risk. Matrix metalloproteinase-9 (MMP-9) is responsible for matrix degradation, cancer invasion and metastasis. Whether areca nut extract (ANE), a BQ component, stimulates MMP-9 secretion, and the related signaling pathways awaits investigation.Results: ANE (but not arecoline) stimulated MMP-9 production of gingival keratinocytes and SAS cancer epithelial cells. ANE stimulated TGF-&#x3B2;1, p-Smad2, and p-TAK1 protein expression. ANE-induced MMP-9 production/expression in SAS cells can be attenuated by SB431542 (ALK5/Smad2 inhibitor), 5Z-7-Oxozeaenol (TAK1 inhibitor), catalase, PD153035 (EGFR tyrosine kinase inhibitor), AG490 (JAK inhibitor), U0126 (MEK/ERK inhibitor), LY294002 (PI3K/Akt inhibitor), betel leaf (PBL) extract, and hydroxychavicol (HC, a PBL component), and melatonin, but not by aspirin.Conclusions: AN components contribute to oral carcinogenesis by stimulating MMP-9 secretion, thus enhancing tumor invasion/metastasis. These events are related to reactive oxygen species, TGF-&#x3B2;1, Smad2-dependent and &#x2013;independent signaling, but not COX. These signaling molecules can be biomarkers of BQ carcinogenesis. PBL, HC and melatonin and other targeting therapy can be used for oral cancer treatment.Methods: ANE-induced MMP-9 expression/secretion of oral epithelial cells and related TGF-&#x3B2;1, Smad-dependent and &#x2013;independent signaling were studied by MTT assay, RT-PCR, western blotting, immunofluorescent staining, and ELISA.
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Specific DNA methylation markers in the diagnosis and prognosis of esophageal cancer

DaPeng Li, Lei Zhang, YuPeng Liu, HongRu Sun, Justina Ucheojor Onwuka, ZhiGang Zhao, WenJing Tian, Jing Xu, YaShuang Zhao, HongYu Xu,

https://doi.org/10.18632/aging.102569 pp 11640—11658

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Li D, Zhang L, Liu Y, Sun H, Onwuka JU, Zhao Z, Tian W, Xu J, Zhao Y, Xu H, . Specific DNA methylation markers in the diagnosis and prognosis of esophageal cancer. . 11:11640-11658. https://doi.org/10.18632/aging.102569

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                TY  - JOUR
                AU  - Li, DaPeng 
                AU  - Zhang, Lei 
                AU  - Liu, YuPeng 
                AU  - Sun, HongRu 
                AU  - Onwuka, Justina Ucheojor 
                AU  - Zhao, ZhiGang 
                AU  - Tian, WenJing 
                AU  - Xu, Jing 
                AU  - Zhao, YaShuang 
                AU  - Xu, HongYu 
                TI  - Specific DNA methylation markers in the diagnosis and prognosis of esophageal cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102569
                DO  - 10.18632/aging.102569
                SP  - 11640
                EP  - 11658
                PY  - 
                AB  - The early diagnosis and accurate prognosis prediction of esophageal cancer is an essential part of improving survival. However, these diseases lack effective and specific markers. A total of 1,744 samples of HumanMethylation450 data were integrated to identify and validate specific methylation markers for esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC) as well as for Barrett&#x2019;s esophagus (BE) using The Cancer Genome Atlas and the Gene Expression Omnibus. The diagnostic and prognostic methylation classifiers were constructed by moderated t-statistics and the least absolute shrinkage and selection operator method. The diagnostic methylation classifier using 12 CpG sites was constructed in training set (377 samples) that could effectively discriminate samples of BE, EAC, and ESCC from normal tissue (AUC = 0.992), which achieved highly predictive ability in both internal (187 samples, AUC = 0.990) and external validation (184 samples, AUC = 0.978). The prognostic methylation classifier with 3 CpG and 2 CpG sites for EAC and ESCC respectively, could accurately estimate the prognosis of an individual patient and improved the predictive ability of the tumor node metastasis staging system. Overall, our study systematically analyzed large-scale methylation data and provided promising markers for the diagnosis and prognosis of esophageal cancer.
                ER  -

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Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Hongrui Guo, Huan Liu, Zhijie Jian, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li, Xun Wang, Ling Zhao, Yi Geng, Ping Ouyang, Weiming Lai, Zhengli Chen, Chao Huang,

https://doi.org/10.18632/aging.102570 pp 11659—11672

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Guo H, Liu H, Jian Z, Cui H, Fang J, Zuo Z, Deng J, Li Y, Wang X, Zhao L, Geng Y, Ouyang P, Lai W, et al, . Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages. . 11:11659-11672. https://doi.org/10.18632/aging.102570

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                TY  - JOUR
                AU  - Guo, Hongrui 
                AU  - Liu, Huan 
                AU  - Jian, Zhijie 
                AU  - Cui, Hengmin 
                AU  - Fang, Jing 
                AU  - Zuo, Zhicai 
                AU  - Deng, Junliang 
                AU  - Li, Yinglun 
                AU  - Wang, Xun 
                AU  - Zhao, Ling 
                AU  - Geng, Yi 
                AU  - Ouyang, Ping 
                AU  - Lai, Weiming 
                AU  - Chen, Zhengli 
                AU  - Huang, Chao 
                TI  - Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102570
                DO  - 10.18632/aging.102570
                SP  - 11659
                EP  - 11672
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Guo, Hongrui 
                AU  - Liu, Huan 
                AU  - Jian, Zhijie 
                AU  - Cui, Hengmin 
                AU  - Fang, Jing 
                AU  - Zuo, Zhicai 
                AU  - Deng, Junliang 
                AU  - Li, Yinglun 
                AU  - Wang, Xun 
                AU  - Zhao, Ling 
                AU  - Geng, Yi 
                AU  - Ouyang, Ping 
                AU  - Lai, Weiming 
                AU  - Chen, Zhengli 
                AU  - Huang, Chao 
                TI  - Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102570
                DO  - 10.18632/aging.102570
                SP  - 11659
                EP  - 11672
                PY  - 
                AB  - Nickel (Ni), an environmental hazard, widely causes allergic contact hypersensitivity worldwide. Despite that Ni-stimulated pro-inflammatory response is vital in allergy, the underlying molecular mechanisms remain largely unclear. Here, we demonstrated that NiCl2 activated nuclear factor kappa B (NF-&#x3BA;B), mitogen-activated protein kinases (MAPKs) and interferon regulatory factor 3 (IRF3) signaling pathways in primary bone marrow-derived macrophages (BMDMs), leading to the altered transcription levels of interleukin-1&#x3B2; (IL-1&#x3B2;), -6, -8, -18, tumor necrosis factor-&#x3B1; (TNF-&#x3B1;) and interferon &#x3B2; (INF-&#x3B2;). We also found that nickel chloride (NiCl2) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1&#x3B2;. NiCl2 induced the accumulation of mitochondrial reactive oxygen species (mtROS) and the release of mitochondrial DNA (mtDNA), thus activating NLRP3 inflammasome pathway. Additionally, NiCl2-induced apoptosis was dependent on the generation of mtROS, and caspase-1 activation might also partly contribute to the apoptotic process. Altogether, abovementioned results indicate that NiCl2 induces inflammatory activation in BMDMs via NF-&#x3BA;B, MAPKs, IRF3 signaling pathways as well as NLRP3 inflammasome pathway, which provides a mechanism to improve the efficiency of treatment against Ni-induced allergic reactions.
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Identification of molecular correlations of RBM8A with autophagy in Alzheimer's disease

Donghua Zou, Rongjie Li, Xiaohua Huang, Guoying Chen, Ying Liu, Youshi Meng, Yimei Wang, Yuan Wu, Yingwei Mao,

https://doi.org/10.18632/aging.102571 pp 11673—11685

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Zou D, Li R, Huang X, Chen G, Liu Y, Meng Y, Wang Y, Wu Y, Mao Y, . Identification of molecular correlations of RBM8A with autophagy in Alzheimer's disease. . 11:11673-11685. https://doi.org/10.18632/aging.102571

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                TY  - JOUR
                AU  - Zou, Donghua 
                AU  - Li, Rongjie 
                AU  - Huang, Xiaohua 
                AU  - Chen, Guoying 
                AU  - Liu, Ying 
                AU  - Meng, Youshi 
                AU  - Wang, Yimei 
                AU  - Wu, Yuan 
                AU  - Mao, Yingwei 
                TI  - Identification of molecular correlations of RBM8A with autophagy in Alzheimer's disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102571
                DO  - 10.18632/aging.102571
                SP  - 11673
                EP  - 11685
                PY  - 
                AB  - Our previous studies revealed RBM8A may play a role in various progressive neurological diseases. The present study aimed to explore the role of RBM8A in Alzheimer&apos;s disease (AD). RBM8A is significantly down-regulated in AD. Interestingly, 9186 differentially expressed genes are overlapped from comparisons of AD versus control and RBM8A-low versus RBM8A-high. Weight gene correlation analysis was performed and 9 functional modules were identified. Modules positively correlated with AD and RBM8A-low are significantly involved in the RAP1 signaling pathway, PI3K&#x2212;AKT signaling pathway, hematopoietic cell lineage, autophagy and APELIN signaling pathway. Fifteen genes (RBM8A, RHBDF2, TNFRSF10B, ACP1, ANKRD39, CA10, CAMK4, CBLN4, LOC284214, NOVA1, PAK1, PPEF1, RGS4, TCEB1 and TMEM118) are identified as hub genes, and the hub gene-based LASSO model can accurately predict the occurrence of AD (AUC = 0.948). Moreover, the RBM8A-module-pathway network was constructed, and low expression of RBM8A down-regulates multiple module genes, including FIP200, Beclin 1, NRBF2, VPS15 and ATG12, which composes key complexes of autophagy. Thus, our study supports that low expression of RBM8A correlates with the decrease of the components of key complexes in autophagy, which could potentially contribute to pathophysiological changes of AD.
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Cytological and genetic consequences for the progeny of a mitotic catastrophe provoked by Topoisomerase II deficiency

Cristina Ramos-Pérez, Margaret Dominska, Laura Anaissi-Afonso, Sara Cazorla-Rivero, Oliver Quevedo, Isabel Lorenzo-Castrillejo, Thomas D. Petes, Félix Machín,

https://doi.org/10.18632/aging.102573 pp 11686—11721

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Ramos-Pérez C, Dominska M, Anaissi-Afonso L, Cazorla-Rivero S, Quevedo O, Lorenzo-Castrillejo I, Petes TD, Machín F, . Cytological and genetic consequences for the progeny of a mitotic catastrophe provoked by Topoisomerase II deficiency. . 11:11686-11721. https://doi.org/10.18632/aging.102573

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                TY  - JOUR
                AU  - Ramos-Pérez, Cristina 
                AU  - Dominska, Margaret 
                AU  - Anaissi-Afonso, Laura 
                AU  - Cazorla-Rivero, Sara 
                AU  - Quevedo, Oliver 
                AU  - Lorenzo-Castrillejo, Isabel 
                AU  - Petes, Thomas D. 
                AU  - Machín, Félix 
                TI  - Cytological and genetic consequences for the progeny of a mitotic catastrophe provoked by Topoisomerase II deficiency
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102573
                DO  - 10.18632/aging.102573
                SP  - 11686
                EP  - 11721
                PY  - 
                AB  - Topoisomerase II (Top2) removes topological linkages between replicated chromosomes. Top2 inhibition leads to mitotic catastrophe (MC) when cells unsuccessfully try to split their genetic material between the two daughter cells. Herein, we have characterized the fate of these daughter cells in the budding yeast. Clonogenic and microcolony experiments, in combination with vital and apoptotic stains, showed that 75% of daughter cells become senescent in the short term; they are unable to divide but remain alive. Decline in cell vitality then occurred, yet slowly, uncoordinatedly when comparing pairs of daughters, and independently of the cell death mediator Mca1/Yca1. Furthermore, we showed that senescence can be modulated by ploidy, suggesting that gross chromosome imbalances during segregation may account for this phenotype. Indeed, we found that diploid long-term survivors of the MC are prone to genomic imbalances such as trisomies, uniparental disomies and terminal loss of heterozygosity (LOH), the latter affecting the longest chromosome arms.
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Histone proteomics reveals novel post-translational modifications in breast cancer

Angela Mena Perri, Valter Agosti, Erika Olivo, Antonio Concolino, MariaTeresa De Angelis, Laura Tammè, Claudia Vincenza Fiumara, Giovanni Cuda, Domenica Scumaci,

https://doi.org/10.18632/aging.102577 pp 11722—11755

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Perri AM, Agosti V, Olivo E, Concolino A, Angelis MD, Tammè L, Fiumara CV, Cuda G, Scumaci D, . Histone proteomics reveals novel post-translational modifications in breast cancer. . 11:11722-11755. https://doi.org/10.18632/aging.102577

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                TY  - JOUR
                AU  - Perri, Angela Mena 
                AU  - Agosti, Valter 
                AU  - Olivo, Erika 
                AU  - Concolino, Antonio 
                AU  - Angelis, MariaTeresa De 
                AU  - Tammè, Laura 
                AU  - Fiumara, Claudia Vincenza 
                AU  - Cuda, Giovanni 
                AU  - Scumaci, Domenica 
                TI  - Histone proteomics reveals novel post-translational modifications in breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102577
                DO  - 10.18632/aging.102577
                SP  - 11722
                EP  - 11755
                PY  - 
                AB  - Histones and their variants are subjected to several post-translational modifications (PTMs). Histones PTMs play an important role in the regulation of gene expression and are critical for the development and progression of many types of cancer, including breast cancer. In this study, we used two-dimensional TAU/SDS electrophoresis, coupled with mass spectrometry for a comprehensive profiling of histone PTMs in breast cancer cell lines.Proteomic approach allowed us to identify 85 histone PTMs, seventeen of which are not reported in the UniProt database. Western blot analysis was performed to confirm a peculiar pattern of PTMs in the sporadic and hereditary breast cancer cell lines compared to normal cells. Overlapping mass spectrometry data with western blotting results, we identified, for the first time to our knowledge, a tyrosine phosphorylation on histone H1, which is significantly higher in breast cancer cells. Additionally, by inhibiting specific signaling paths, such as PI3K, PPAR&#x3B3; and FAK pathways, we established a correlation between their regulation and the presence of new histone PTMs. Our results may provide new insight on the possible implication of these modifications in breast cancer and may offer new perspectives for future clinical applications.
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Adipose-derived stem cells contribute to cardiovascular remodeling

Hui Ni, Yiming Zhao, Yongli Ji, Jian Shen, Meixiang Xiang, Yao Xie,

https://doi.org/10.18632/aging.102491 pp 11756—11769

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Ni H, Zhao Y, Ji Y, Shen J, Xiang M, Xie Y, . Adipose-derived stem cells contribute to cardiovascular remodeling. . 11:11756-11769. https://doi.org/10.18632/aging.102491

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                TY  - JOUR
                AU  - Ni, Hui 
                AU  - Zhao, Yiming 
                AU  - Ji, Yongli 
                AU  - Shen, Jian 
                AU  - Xiang, Meixiang 
                AU  - Xie, Yao 
                TI  - Adipose-derived stem cells contribute to cardiovascular remodeling
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102491
                DO  - 10.18632/aging.102491
                SP  - 11756
                EP  - 11769
                PY  - 
                AB  - Obesity is an independent risk factor for cardiovascular disease. Adipose tissue was initially thought to be involved in metabolism through paracrine. Recent researches discovered mesenchymal stem cells inside adipose tissue which could differentiate into vascular lineages in vitro and in vivo, participating vascular remodeling. However, there were few researches focusing on distinct characteristics and functions of adipose-derived stem cells (ADSCs) from different regions. This is the first comprehensive review demonstrating the variances of ADSCs from the perspective of their origins.
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Cancer stem cells-driven tumor growth and immune escape: the Janus face of neurotrophins

Viviana Triaca, Valentina Carito, Elena Fico, Pamela Rosso, Marco Fiore, Massimo Ralli, Alessandro Lambiase, Antonio Greco, Paola Tirassa,

https://doi.org/10.18632/aging.102499 pp 11770—11792

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Triaca V, Carito V, Fico E, Rosso P, Fiore M, Ralli M, Lambiase A, Greco A, Tirassa P, . Cancer stem cells-driven tumor growth and immune escape: the Janus face of neurotrophins. . 11:11770-11792. https://doi.org/10.18632/aging.102499

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                TY  - JOUR
                AU  - Triaca, Viviana 
                AU  - Carito, Valentina 
                AU  - Fico, Elena 
                AU  - Rosso, Pamela 
                AU  - Fiore, Marco 
                AU  - Ralli, Massimo 
                AU  - Lambiase, Alessandro 
                AU  - Greco, Antonio 
                AU  - Tirassa, Paola 
                TI  - Cancer stem cells-driven tumor growth and immune escape: the Janus face of neurotrophins
                JO  - 
                JA  - 
                VL  - 11
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102499
                DO  - 10.18632/aging.102499
                SP  - 11770
                EP  - 11792
                PY  - 
                AB  - Cancer Stem Cells (CSCs) are self-renewing cancer cells responsible for expansion of the malignant mass in a dynamic process shaping the tumor microenvironment. CSCs may hijack the host immune surveillance resulting in typically aggressive tumors with poor prognosis.In this review, we focus on neurotrophic control of cellular substrates and molecular mechanisms involved in CSC-driven tumor growth as well as in host immune surveillance. Neurotrophins have been demonstrated to be key tumor promoting signaling platforms. Particularly, Nerve Growth Factor (NGF) and its specific receptor Tropomyosin related kinase A (TrkA) have been implicated in initiation and progression of many aggressive cancers. On the other hand, an active NGF pathway has been recently proven to be critical to oncogenic inflammation control and in promoting immune response against cancer, pinpointing possible pro-tumoral effects of NGF/TrkA-inhibitory therapy.A better understanding of the molecular mechanisms involved in the control of tumor growth/immunoediting is essential to identify new predictive and prognostic intervention and to design more effective therapies. Fine and timely modulation of CSCs-driven tumor growth and of peripheral lymph nodes activation by the immune system will possibly open the way to precision medicine in neurotrophic therapy and improve patient&#x2019;s prognosis in both TrkA- dependent and independent cancers.
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Correction for: Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice

Luis Miguel Guachalla, Zhenyu Ju, Rafal Koziel, Guido von Figura, Zhangfa Song, Markus Fusser, Bernd Epe, Pidder Jansen-Dürr, K. Lenhard Rudolph,

https://doi.org/10.18632/aging.102602 pp 11793—11794

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Guachalla LM, Ju Z, Koziel R, von Figura G, Song Z, Fusser M, Epe B, Jansen-Dürr P, Rudolph KL, . Correction for: Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice. . 11:11793-11794. https://doi.org/10.18632/aging.102602

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Volume 11, Issue 23

About the Cover

Editorials

Marc R. Benoit, Manoshi Gayen, Riqiang Yan,

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Anders Dahl, José M. Miro, Niels E. Bruun,

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Julius L. Katzmann, Ulrich Laufs,

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Laurien E. Zijlstra, Simon P. Mooijaart, J. Wouter Jukema,

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Xavier Deschênes-Simard, Marie-Camille Rowell, Gerardo Ferbeyre,

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Research Papers

Hongbin Chen, Wei Lin, Peiqiang Lin, Mouwei Zheng, Yongxing Lai, Manli Chen, Yixian Zhang, Jianhao Chen, Xiaohui Lin, Longzai Lin, Quan Lan, Qilin Yuan, Ronghua Chen, Xinhong Jiang, Yingchun Xiao, Nan Liu,

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Kunchi Zhao, Yang Zhang, Hongping Yuan, Mingming Zhao, Dongxu Zhao,

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Yinjie Su, Zehu Du, Guanglei Zhong, Yiyao Ya, Junming Bi, Juanyi Shi, Luping Chen, Wen Dong, Tianxin Lin,

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Jianxu Chen, Jiandi Chen, Jiaxin Huang, Zhanyu Li, Yihang Gong, Baojia Zou, Xialei Liu, Lei Ding, Peiping Li, Zhiquan Zhu, Baimeng Zhang, Hui Guo, Chaonong Cai, Jian Li,

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Longyang Jiang, Lan Zhao, Jia Bi, Qiutong Guan, Aoshuang Qi, Qian Wei, Miao He, Minjie Wei, Lin Zhao,

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Yunjie He, Siying Zhou, Fei Deng, Shujie Zhao, Wenquan Chen, Dandan Wang, Xiu Chen, Juncheng Hou, Jian Zhang, Wei Zhang, Li Ding, Jinhai Tang, Zuomin Zhou,

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Rui Zhang, Yuan Liu, Hui Liu, Wei Chen, Hui-Ning Fan, Jing Zhang, Jin-Shui Zhu,

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Xiang-Yu Zheng, Yu-Dan Lv, Feng-Yan Jin, Xiu-Juan Wu, Jie Zhu, Yang Ruan,

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Ling-Zhi Ma, Yu-Yuan Huang, Zuo-Teng Wang, Jie-Qiong Li, Xiao-He Hou, Xue-Ning Shen, Ya-Nan Ou, Qiang Dong, Lan Tan, Jin-Tai Yu, Alzheimer’s Disease Neuroimaging Initiative,

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Hui Sun, Ting-Ting Gong, Yu-Ting Jiang, Shuang Zhang, Yu-Hong Zhao, Qi-Jun Wu,

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Kun Ren, Heng Li, Hui-Fang Zhou, Yin Liang, Min Tong, Lu Chen, Xi-Long Zheng, Guo-Jun Zhao,

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Nian Tan, Jianwei Liu, Ping Li, Zhaoying Sun, Jianming Pan, Wei Zhao,

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Kan Sun, Diaozhu Lin, Qiling Feng, Feng Li, Yiqin Qi, Chulin Huang, Wanting Feng, Chuan Yang, Li Yan, Meng Ren,

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Chao-Qun Wang, Chih-Yang Lin, Yuan-Li Huang, Shih-Wei Wang, Yan Wang, Bi-Fei Huang, Yu-Wei Lai, Shun-Long Weng, Yi-Chin Fong, Chih-Hsin Tang, Zhong Lv,

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