@Article{096504020X15954139263808,
AUTHOR = {Junfeng Lu, Zhongsong Zhao, Yanhong Ma},
TITLE = {miR-186 Represses Proliferation, Migration, Invasion, and EMT  of Hepatocellular Carcinoma via Directly Targeting CDK6},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {5},
PAGES = {509--518},
URL = {http://www.techscience.com/or/v28n5/48510},
ISSN = {1555-3906},
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.},
DOI = {10.3727/096504020X15954139263808}
}