Construction and analysis of cardiac hypertrophy-associated lncRNA-mRNA network based on competitive endogenous RNA reveal functional lncRNAs in cardiac hypertrophy

// Chao Song 1,* , Jian Zhang 2,* , Yan Liu 1 , Hao Pan 1 , Han-ping Qi 1 , Yong-gang Cao 1 , Jian-mei Zhao 2 , Shang Li 2 , Jing Guo 1 , Hong-li Sun 1 and Chun-quan Li 2 1 Department of Pharmacology, Harbin Medical University-Daqing, Daqing, China 2 Department of Medical Informatics, Harbin Medical University-Daqing, Daqing, China * These authors have contributed equally to this work Correspondence to: Hong-li Sun, email: // Chun-quan Li, email: // Keywords : cardiac hypertrophy, lncRNA, ceRNA, gene expression profile, network analysis, Pathology Section Received : October 21, 2015 Accepted : January 28, 2016 Published : February 10, 2016 Abstract Cardiac hypertrophy (CH) could increase cardiac after-load and lead to heart failure. Recent studies have suggested that long non-coding RNA (lncRNA) played a crucial role in the process of the cardiac hypertrophy, such as Mhrt, TERMINATOR. Some studies have further found a new interacting mechanism, competitive endogenous RNA (ceRNA), of which lncRNA could interact with micro-RNAs (miRNA) and indirectly interact with mRNAs through competing interactions. However, the mechanism of ceRNA regulated by lncRNA in the CH remained unclear. In our study, we generated a global triple network containing mRNA, miRNA and lncRNA, and extracted a CH related lncRNA-mRNA network (CHLMN) through integrating the data from starbase, miRanda database and gene expression profile. Based on the ceRNA mechanism, we analyzed the characters of CHLMN and found that 3 lncRNAs (SLC26A4-AS1, RP11-344E13.3 and MAGI1-IT1) were high related to CH. We further performed cluster module analysis and random walk with restart for the CHLMN, finally 14 lncRNAs had been discovered as the potential CH related disease genes. Our results showed that lncRNA played an important role in the CH and could shed new light to the understanding underlying mechanisms of the CH.