Open AccessmiR-186 Represses Proliferation, Migration, Invasion, and EMT of Hepatocellular Carcinoma via Directly Targeting CDK6
Author(s) -
Junfeng Lu,
Zhongsong Zhao,
Yue Ma
Publication year - 2020
Publication title -
oncology research
Language(s) - English
Resource type - Journals
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504020x15954139263808
Subject(s) - cyclin dependent kinase 6 , cancer research , apoptosis , cell growth , hepatocellular carcinoma , cell migration , biology , cyclin d1 , cell cycle , cell , biochemistry , genetics
The present study aimed to investigate the effect of miR-186 on proliferation, migration, invasion, and epithelialmesenchymal transition (EMT) of hepatocellular carcinoma (HCC). In this work, miR-186 was downregulated in HCC tissues and cells, and low miR-186 level helped predict the occurrence of vascular invasion and poor prognosis in patients with HCC. miR-186 overexpression inhibited cell proliferation and tumor growth in nude mice, repressed migration and invasion abilities, and enhanced apoptosis in HCC cells. miR-186 also retarded progression of EMT. miR-186 directly bound to the 3-untranslated regions of cyclin-dependent kinase 6 (CDK6) to inhibit its expression. Overexpression of CDK6 markedly reversed inhibitory effects of miR-186 on proliferation, apoptosis, migration, and invasion of HCC cells. Conversely, inhibition of CDK6 exerted synergic effect on the biological functions of miR-186. In conclusion, miR-186 represses proliferation, migration, invasion, and EMT, and induces apoptosis through targeting CDK6 in HCC, which may provide a new therapeutic target for HCC.