Published online Nov 7, 2015. doi: 10.3748/wjg.v21.i41.11680
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
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.