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

被引:10
|
作者
Lu, Junfeng [1 ]
Zhao, Zhongsong [2 ]
Ma, Yanhong [3 ]
机构
[1] Shandong Univ, Cheeloo Coll Med, Shandong Prov Hosp 3, Dept Vasc Surg, Jinan, Peoples R China
[2] Shandong Univ, Cheeloo Coll Med, Shandong Prov Hosp 3, Dept Gastroenterol, Jinan, Peoples R China
[3] Shandong Univ, Cheeloo Coll Med, Shandong Prov Hosp 3, Dept Ultrasound, 11 Cent Wuying Hill Rd, Jinan 250031, Shandong, Peoples R China
关键词
miR-186; Cyclin-dependent kinase 6 (CDK6); Epithelial-mesenchymal transition (EMT); Hepatocellular carcinoma (HCC); CELL-PROLIFERATION; CANCER; METASTASIS; INHIBITION; MICRORNAS; CYCLE; ERA;
D O I
10.3727/096504020X15954139263808
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:509 / 518
页数:10
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