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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Wu, Cheng-lin Mao, Ze-bin Wang, Yu Jin, Bo Chen, Hao Xie, Bu-shan |
| Description | Author Affiliation: Wu CL ( From the Department of Biochemistry and Molecular Biology and Beijing Key Laboratory for 'Posttranslational Modification and Cellular Function,' Health Science Center, Peking University, 38 Xueyuan Road, Beijing 100191, China.); Wang Y ( the Departments of Urology and Microbiology, New York University Medical Center, New York, New York 10016, and.); Jin B ( From the Department of Biochemistry and Molecular Biology and Beijing Key Laboratory for 'Posttranslational Modification and Cellular Function,' Health Science Center, Peking University, 38 Xueyuan Road, Beijing 100191, China.); Chen H ( From the Department of Biochemistry and Molecular Biology and Beijing Key Laboratory for 'Posttranslational Modification and Cellular Function,' Health Science Center, Peking University, 38 Xueyuan Road, Beijing 100191, China.); Xie BS ( the Department of Gastroenterology, First Affiliated Hospital of Nanchang University, 17 Yongwai Zheng Street, Nanchang 330000, China.); Mao ZB ( From the Department of Biochemistry and Molecular Biology and Beijing Key Laboratory for 'Posttranslational Modification and Cellular Function,' Health Science Center, Peking University, 38 Xueyuan Road, Beijing 100191, China, zbmao@bjmu.edu.cn.) |
| Abstract | Long non-coding RNAs (lncRNAs) have recently emerged as key players in many physiologic and pathologic processes. Although many lncRNAs have been identified, few lncRNAs have been characterized functionally in aging. In this study, we used human fibroblast cells to investigate genome-wide lncRNA expression during cellular senescence. We identified 968 down-regulated lncRNAs and 899 up-regulated lncRNAs in senescent cells compared with young cells. Among these lncRNAs, we characterized a senescence-associated lncRNA (SALNR), whose expression was reduced during cellular senescence and in premalignant colon adenomas. Overexpression of SALNR delayed cellular senescence in fibroblast cells. Furthermore, we found that SALNR interacts with NF90 (nuclear factor of activated T-cells, 90 kDa), an RNA-binding protein suppressing miRNA biogenesis. We demonstrated that NF90 is a SALNR downstream target, whose inhibition led to premature senescence and enhanced expressions of senescence-associated miRNAs. Moreover, our data showed that Ras-induced stress promotes NF90 nucleolus translocation and suppresses its ability to suppress senescence-associated miRNA biogenesis, which could be rescued by SALNR overexpression. These data suggest that lncRNA SALNR modulates cellular senescence at least partly through changing NF90 activity. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 50 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-12-11 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cell Aging Genetics Nuclear Factor 90 Proteins Physiology Oncogenes RNA, Long Noncoding Cell Nucleolus Metabolism Cells, Cultured Genome-Wide Association Study Protein Transport Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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