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MiR-502-3P suppresses cell proliferation, migration, and invasion in hepatocellular carcinoma by targeting SET

Authors Jin H, Yu M, Lin Y, Hou B, Wu Z, Li Z, Sun J

Received 23 April 2015

Accepted for publication 19 October 2015

Published 31 May 2016 Volume 2016:9 Pages 3281—3289

DOI https://doi.org/10.2147/OTT.S87183

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Nitin Kumar Agarwal

Peer reviewer comments 4

Editor who approved publication: Dr Faris Farassati


Haosheng Jin,* Min Yu,* Ye Lin, Baohua Hou, Zhongshi Wu, Zhide Li, Jian Sun

Department of General Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, People’s Republic of China

*These authors contributed equally to this work

Background/aim: Increasing evidences show that microRNAs are engaged in hepatocellular carcinoma (HCC). The aim of this study was to investigate the role of miR-502-3P in HCC and to identify its underlying mechanism.
Methods: The expression levels of miR-502-3P were assessed in multiple HCC cell lines and in liver tissues of patients with HCC. We further examined the effects of miR-502-3P on malignant behavior of HCC. The molecular target of miR-502-3P was identified using a computer algorithm and confirmed experimentally.
Results: Downregulation of miR-502-3P was found in both HCC cell lines and human samples. Overexpression of miR-502-3P dramatically inhibits HCC proliferation, metastasis, invasion, and cell adhesion. We further verify the SET as a novel and direct target of miR-502-3P in HCCs.
Conclusion: Taken together, overexpression of miR-502-3P or downregulation of SET may prove beneficial as a therapeutic strategy for HCC treatment.

Keywords: miRNA, HCC, SET gene, recurrence

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