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Copyright ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 7, 2020; 26(29): 4240-4260
Published online Aug 7, 2020. doi: 10.3748/wjg.v26.i29.4240
Role of long noncoding RNA-mediated competing endogenous RNA regulatory network in hepatocellular carcinoma
Zhao-Shan Niu, Wen-Hong Wang, Xian-Ning Dong, Li-Mei-Li Tian
Zhao-Shan Niu, Laboratory of Micromorphology, School of Basic Medicine, Medical Department of Qingdao University, Qingdao 266071, Shandong Province, China
Wen-Hong Wang, Department of Pathology, School of Basic Medicine, Medical Department of Qingdao University, Qingdao 266071, Shandong Province, China
Xian-Ning Dong, Department of Pathology, the Affiliated Hospital of Qingdao University, Qingdao 266061, Shandong Province, China
Li-Mei-Li Tian, BGI Gene Innovation Class, School of Basic Medicine, Medical Department of Qingdao University, Qingdao 266071, Shandong Province, China
Author contributions: Niu ZS designed, wrote, edited, and revised the manuscript; Wang WH, Dong XN, and Tian LML reviewed the scientific literature in the field.
Conflict-of-interest statement: The authors declare no conflict of interests.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Zhao-Shan Niu, MD, Associate Professor, Laboratory of Micromorphology, School of Basic Medicine, Medical Department of Qingdao University, Room 1109, Medical Education Complex-Building B, No. 1 Ningde Road, Qingdao 266071, Shandong Province, China. z.s.niu@qdu.edu.cn
Received: April 13, 2020
Peer-review started: April 13, 2020
First decision: June 18, 2020
Revised: July 5, 2020
Accepted: July 15, 2020
Article in press: July 15, 2020
Published online: August 7, 2020
Abstract

Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are noncoding RNAs (ncRNAs) that occupy over 90% of the human genome, and their main function is to directly or indirectly regulate messenger RNA (mRNA) expression and participate in the tumorigenesis and progression of malignances. In particular, some lncRNAs can interact with miRNAs as competing endogenous RNAs (ceRNAs) to modulate mRNA expression. Accordingly, these RNA molecules are interrelated and coordinate to form a dynamic lncRNA-mediated ceRNA regulatory network. Mounting evidence has revealed that lncRNAs that act as ceRNAs are closely related to tumorigenesis. To date, numerous studies have established many different regulatory networks in hepatocellular carcinoma (HCC), and perturbations in these ceRNA interactions may result in the initiation and progression of HCC. Herein, we emphasize recent advances concerning the biological function of lncRNAs as ceRNAs in HCC, with the aim of elucidating the molecular mechanism underlying these HCC-related RNA molecules and providing novel insights into the diagnosis and treatment of HCC.

Keywords: Hepatocellular carcinoma, Long noncoding RNA, MicroRNA, Competing endogenous RNA, Function, Mechanism

Core tip: Mounting evidence has revealed that long noncoding RNA (lncRNA)-mediated competitive endogenous RNA (ceRNA) regulatory network plays a crucial role in tumorigenesis. To date, numerous studies have established many different regulatory networks in hepatocellular carcinoma (HCC), and perturbations in these ceRNA interactions may result in the initiation and progression of HCC. Herein, we emphasize recent advances concerning the biological function of lncRNAs as ceRNAs in HCC, with the aim of elucidating the molecular mechanism underlying these HCC-related RNA molecules and providing novel insights into the diagnosis and treatment of HCC.