Open Access

ARTICLE

miR-186 Represses Proliferation, Migration, Invasion, and EMT of Hepatocellular Carcinoma via Directly Targeting CDK6

Junfeng Lu^*, Zhongsong Zhao^†, Yanhong Ma^‡

* Department of Vascular Surgery, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Jinan, P.R. China
† Department of Gastroenterology, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Jinan, P.R. China
‡ Department of Ultrasound, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Jinan, P.R. China

Oncology Research 2020, 28(5), 509-518. https://doi.org/10.3727/096504020X15954139263808

Abstract

The present study aimed to investigate the effect of miR-186 on proliferation, migration, invasion, and epithelial–mesenchymal 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.

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Keywords

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