Methylation‐mediated miR‐214 regulates proliferation and drug sensitivity of renal cell carcinoma cells through targeting LIVIN. Issue 11 (12th May 2020)

• Record Type: Journal Article
• Authors: Xu, Hao; Wu, Shangjun; Shen, Xin; Shi, Zhan; Wu, Ding; Yuan, Yuan; Jiang, Wei; Wang, Qianliang; Ke, Qin; Mao, Qing; Li, Xianlong; Liu, Yong; Yuan, Pingcheng; Zhang, Qinghan; Huang, Enying; Chen, Xiaogang
• Is Part Of: Journal of cellular and molecular medicine. Volume 24:Issue 11(2020)
• Page Start: 6410
• Page End: 6425
• Publication Date: 2020-05-12
• Subjects: chemotherapy -- DNMT1 -- LIVIN -- methylation -- miR‐214 -- RCC; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.15287
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: LIVIN, a member of the inhibitor of apoptosis proteins (IAPs), is reported playing important roles in the development and progression of multiple human cancers. However, its underlined mechanisms in human renal cell carcinoma (RCC) are still needed to be clarified. In the present study, we reported that inhibition of miR‐214 promoted the expression of LIVIN, then facilitated RCC cells growth and reduced the sensitivity of RCC cells to chemotherapeutic drugs. In constant, overexpression of miR‐214 had contradictory effects. Further investigation showed that miR‐214 was down‐regulated in RCC because of abnormal methylation. In addition, DNA methyltransferase DNMT1, miR‐214 and LIVIN are directly correlated in RCC patients. In conclusion, these results suggest that abnormal miR‐214 methylation negatively regulates LIVIN, which may promote RCC cells growth and reduced the sensitivity of RCC cells to chemotherapeutic drugs.