Basic Study
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 21, 2015; 21(23): 7208-7217
Published online Jun 21, 2015. doi: 10.3748/wjg.v21.i23.7208
Long noncoding RNAs in hepatitis B virus-related hepatocellular carcinoma
Ting-Ting Yu, Xi-Ming Xu, Yi Hu, Jun-Jian Deng, Wei Ge, Na-Na Han, Mei-Xia Zhang
Ting-Ting Yu, Xi-Ming Xu, Yi Hu, Jun-Jian Deng, Wei Ge, Na-Na Han, Mei-Xia Zhang, Cancer Center, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
Author contributions: Yu TT and Xu XM contributed equally to this work; Yu TT, Xu XM, Hu Y, and Deng JJ designed research; Yu TT, Ge W, Han NN, and Zhang MX performed research; Yu TT, Han NN, and Zhang MX analyzed data; Yu TT and Xu XM wrote the paper.
Ethics approval: The study was approved by the Human Research Ethics Committee of Renmin Hospital of Wuhan University.
Conflict-of-interest: There are no conflicts of interest.
Data sharing: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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/
Correspondence to: Xi-Ming Xu, MD, PhD, Cancer Center, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuhan 430060, Hubei Province, China. vipdoctorxu@163.com
Telephone: +86-27-88042292 Fax: +86-27-88042292
Received: November 19, 2014
Peer-review started: November 19, 2014
First decision: December 11, 2014
Revised: December 26, 2014
Accepted: March 27, 2015
Article in press: March 27, 2015
Published online: June 21, 2015
Abstract

AIM: To study the expression of long noncoding RNAs (lncRNAs) in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC).

METHODS: The lncRNA profiles between HBV-related HCC tissues and corresponding normal liver tissues were generated using microarray analysis. Datasets were analyzed using multiple algorithms to depict alterations in gene expression on the basis of gene ontology (GO), pathway analysis, and lncRNA levels.

RESULTS: The microarray revealed that 1772 lncRNAs and 2508 mRNAs were differently expressed. The pathway analysis demonstrated that the cell cycle, cytokine-cytokine receptor interaction, chemokine signaling pathway, and phosphoinositide 3-kinase-protein kinase B signaling pathway may play important roles in HCC. Several GO terms, such as cell cycle, DNA replication, immune response, and signal transduction, were enriched in gene lists, suggesting a potential correlation with HBV-related HCC. The upregulated large intergenic noncoding RNA ULK4P2 was physically combined with enhancer of zeste homolog 2. Therefore, the lncRNAs may participate in regulating HBV-related HCC.

CONCLUSION: lncRNAs play important roles in HCC, future studies should verify whether large intergenic noncoding ULK4P2 functions by combining with enhancer of zeste homolog 2 in HCC.

Keywords: Enhancer of zeste homolog 2, Hepatocellular carcinoma, Long noncoding RNAs, Microarray, ULK4P2

Core tip: This manuscript examines the differential expression of long noncoding RNAs in hepatitis B virus-related hepatocellular carcinoma using gene ontology and pathway analyses, and constructing a long noncoding RNA-mRNA network to research the data. Furthermore, RNA immunoprecipitation revealed that the large intergenic noncoding RNA ULK4P2 physically combined with enhancer of zeste homolog 2 (EZH2). EZH2 plays an important role in many cancer types and is critical for cancer cell proliferation, survival, and metastasis, and drug resistance. The combination of ULK4P2 and EZH2 provides a novel avenue for further study of ULK4P2 in hepatitis B virus-related hepatocellular carcinoma.