MiR‐186 modulates hepatocellular carcinoma cell proliferation and mobility via targeting MCRS1‐mediated Wnt/β‐catenin signaling. Issue 12 (29th May 2019)

• Record Type: Journal Article
• Authors: Wang, Huiling; Ou, Jinrui; Jian, Zhixiang; Ou, Yingliang
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 12(2019:Dec.)
• Page Start: 23135
• Page End: 23145
• Publication Date: 2019-05-29
• Subjects: hepatocellular carcinoma -- invasion -- MCRS1 -- migration -- miR‐186 -- proliferation -- Wnt; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.28878
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Previous studies have revealed that miR‐186 is involved in the pathogenesis of many malignancies. However, the role of miR‐186 in hepatocellular carcinoma (HCC) carcinogenesis and its detailed mechanism are poorly understood. This study was to investigate the function of miR‐186 in modulating HCC cell proliferation, cell cycle, migration, and invasion. We found that miR‐186 was decreased in HCC tissues and cell lines. Loss‐of‐function experiments showed that reduction of miR‐186 dramatically enhanced tumor cell proliferation and metastasis. Besides, miR‐186 also participated in the modulation of the cell cycle. In addition, luciferase reporter assays and Western blot analysis showed that MCRS1 was a novel target of miR‐186 in HCC cells. Notably, upregulation of miR‐186 suppressed the nuclear β‐catenin accumulation and blocked the activation of Wnt/β‐catenin signaling in HCC cells. Forced MCRS1 expression abrogated the inhibitory effect of miR‐186 on cell growth, metastasis and Wnt/β‐catenin signaling in HCC cells. Our findings may provide new insight into the pathogenesis of HCC and miR‐186/ MCRS1 might function as new therapeutic targets for HCC. Abstract : Decreased expression of miR‐186 in hepatocellular carcinoma is responsible for the high expression of MCRS1, followed by the aberrant activation of Wnt/β‐catenin signaling and its downstream targets, which may, in turn, promote proliferation and metastasis.