MiR‐194 functions as a novel modulator of cellular senescence in mouse embryonic fibroblasts. (22nd January 2017)

• Record Type: Journal Article
• Authors: Xu, Shun; Zhang, Bing; Zhu, Yanmei; Huang, Haijiao; Yang, Wenping; Huang, Haiyong; Zheng, Hui‐ling; Liu, Xinguang
• Is Part Of: Cell biology international. Volume 41:Number 3(2017)
• Page Start: 249
• Page End: 257
• Publication Date: 2017-01-22
• Subjects: cellular senescence -- DNMT3A -- miR‐194; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10715
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: MicroRNA‐194 (miR‐194), a typical p53 responsive miRNA, serves as a tumor suppressor similar as p53, and has been demonstrated to play an anti‐proliferation role in various human cancers. In spite of the pivotal role of p53 during aging process, the knowledge of miR‐194's contribution to cellular senescence is limited. We herein sought to explore the role of miR‐194 in the replicative senescence and stress‐induced senescence of mouse embryonic fibroblasts. Our results unraveled that, compared to young cells, miR‐194 is highly expressed in senescent cells, and extra expression of miR‐194 significantly triggers the replicative senescence of MEFs and H2 O2 ‐induced senescence of NIH/3T3 cells, while inhibition of miR‐194 exhibited the opposite effect. We further unveiled that DNMT3A was a direct and authentic target of miR‐194, which has been reported to be closely associated with cellular senescence. Taken together, our data suggest that miR‐194 may significantly promote the development of cellular senescence in mouse embryonic fibroblasts, which potentially occurs through inhibiting the DNMT3A expression.