Guo LL, Song CH, Wang P, Dai LP, Zhang JY, Wang KJ. Competing endogenous RNA networks and gastric cancer. World J Gastroenterol 2015; 21(41): 11680-11687 [PMID: 26556995 DOI: 10.3748/wjg.v21.i41.11680]
Corresponding Author of This Article
Kai-Juan Wang, PhD, Department of Epidemiology and Statistics, College of Public Health, Zhengzhou University, No. 100 Science Avenue, Zhengzhou 450001, Henan Province, China. kjwang@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Topic Highlight
Open-Access Policy of This Article
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/
Lei-Lei Guo, Section of Infection Control of the Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, Henan Province, China
Chun-Hua Song, Peng Wang, Li-Ping Dai, Jian-Ying Zhang, Kai-Juan Wang, Department of Epidemiology and Statistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan Province, China
Author contributions: Guo LL drafted the manuscript; Song CH, Wang P, Dai LP, Zhang JY and Wang KJ provided substantial contributions to conception of the manuscript, and helped draft the article or make critical revisions related to important intellectual content of the manuscript.
Supported by National Nature Science Foundation of China, No. 81373097.
Conflict-of-interest statement: The authors have no conflict of interest related to the manuscript.
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: Kai-Juan Wang, PhD, Department of Epidemiology and Statistics, College of Public Health, Zhengzhou University, No. 100 Science Avenue, Zhengzhou 450001, Henan Province, China. kjwang@163.com
Telephone: +86-371-67781454
Received: April 28, 2015 Peer-review started: May 4, 2015 First decision: July 14, 2015 Revised: August 12, 2015 Accepted: September 15, 2015 Article in press: September 15, 2015 Published online: November 7, 2015 Processing time: 189 Days and 17.6 Hours
Abstract
Recent studies have showed that RNAs regulate each other with microRNA (miRNA) response elements (MREs) and this mechanism is known as “competing endogenous RNA (ceRNA)” hypothesis. Long non-coding RNAs (lncRNAs) are supposed to play important roles in cancer. Compelling evidence suggests that lncRNAs can interact with miRNAs and regulate the expression of miRNAs as ceRNAs. Several lncRNAs such as H19, HOTAIR and MEG3 have been found to be associated with miRNAs in gastric cancer (GC), generating regulatory crosstalk across the transcriptome. These MRE sharing elements implicated in the ceRNA networks (ceRNETs) are able to regulate mRNA expression. The ceRNA regulatory networks including mRNAs, miRNAs, lncRNAs and circular RNAs may play critical roles in tumorigenesis, and the perturbations of ceRNETs may contribute to the pathogenesis of GC.
Core tip: Competitive endogenous RNAs (ceRNAs) share microRNA (miRNA) response elements and compete common miRNAs, thereby regulating each other’s expression. The ceRNA regulatory networks including mRNAs, miRNAs, long non-coding RNAs and circular RNAs play critical roles in tumorigenesis, and the perturbations of ceRNA networks may contribute to the pathogenesis of gastric cancer.
