FAM201A, a long noncoding RNA potentially associated with atrial fibrillation identified by ceRNA network analyses and WGCNA

Author:

Chen Xi,He Xiang-Yu,Dan Qing,Li Yang

Abstract

Abstract Background Being the most common arrhythmia in clinic, atrial fibrillation (AF) causes various comorbidities to patients such as heart failure and stroke. LncRNAs were reported involved in pathogenesis of AF, yet, little is known about AF-associated lncRNAs. The present study aims to explore lncRNAs associated with AF susceptibility based on competing endogenous RNA (ceRNA) network analysis and weighted gene co-expression network analysis (WGCNA). Methods GSE41177 and GSE79768 datasets were obtained from the Gene Expression Omnibus (GEO) database. Competing endogenous RNA (ceRNA) network analysis was performed using GSE41177. Differentially expressed lncRNAs (DElncRNAs), mRNAs (DEmRNAs) between AF patients and patients with sinus rhythm (SR) were identified from GSE41177 using R software. Then, the ceRNA network was constructed based on DElncRNAs, the predicted target miRNAs and DEmRNAs. Weighted gene co-expression network analysis (WGCNA) was performed using GSE79768 to validate the AF-related lncRNAs identified from GSE41177. LncRNA modules and crucial lncRNAs relevant to AF and were identified. Results In summary, 18 DElncRNAs and 350 DEmRNAs were found between AF patients and SR patients. A total of 5 lncRNAs, 10 miRNAs, and 21 mRNAs were contained in the final ceRNA network. Taking into consideration both the ceRNA theory and inference scores from the comparative toxicogenomics database (CTD) database, the ceRNA axis FAM201A-miR-33a-3p-RAC3 was identified as mostly relevant to AF susceptibility. FAM201A (Gene significance, GS = − 0.62; Module membership, MM = 0.75) was also proved in the blue module, which was identified most highly relevant with AF by WGCNA. Conclusions These results demonstrated that decreased expression of FAM201A might be associated with susceptibility of AF. Working as the ceRNA to regulate RAC3 might be one function of FAM201A in AF susceptibility, which requires further exploration in future research.

Funder

National Natural Science Foundation of China

Publisher

Springer Science and Business Media LLC

Subject

Genetics (clinical),Genetics

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