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LINC01296 promotes proliferation, migration, and invasion of HCC cells by targeting miR-122-5P and modulating EMT activity

Authors Wan Y, Li M, Huang P

Received 7 December 2018

Accepted for publication 1 February 2019

Published 26 March 2019 Volume 2019:12 Pages 2193—2203

DOI https://doi.org/10.2147/OTT.S197338

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Dr Sanjeev Srivastava


Yafeng Wan, Molin Li, Ping Huang

National Key Clinical Department, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing 400000, People’s Republic of China

Introduction: Long noncoding RNAs (lncRNAs) play an important role in the origination and progression of hepatocellular carcinoma (HCC). However, the biological function of the long intergenic non-protein-coding RNA, LINC01296, in HCC remains unknown.
Methods: Here, we observed an increase in the expression levels of LINC01296 in HCC tissues and cell lines using reverse transcription quantitative PCR; these data were consistent with that obtained from The Cancer Genome Atlas database.
Results: A higher expression level was correlated with higher alpha fetoprotein levels, a larger tumor size, an advanced TNM stage, and a poorer overall survival rate. Upregulation of LINC01296 promoted the proliferation, migration, and invasion of HCC cells. Improvement of cell migration and invasion attributable to the overexpression of LINC01296 was related to an increase in epithelial–mesenchymal transition (EMT). Mechanistically, miR-122-5P can bind to LINC01296 and decrease its oncogenic effect.
Conclusion: Collectively, the results of this study revealed that LINC01296 is a tumor promoter that can promote the migration and invasion of HCC cells through EMT, while miR-122-5P is involved in the underlying mechanisms.

Keywords: hepatocellular carcinoma, LINC01296, miR-122-5P, EMT

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