Long non-coding RNA BANCR promotes interferon-β-induced cardiomyocyte apoptosis by targeting signal transducer and activator of transcription 1 in vitro.

Myocardium functions as an immune organ, and myocardial ischemia-reperfusion (I/R) is known to initiate myocardial innate immune response to induce myocardial injury. However, the mechanisms underlying interferon-β (IFN-β)-mediated myocardial injury during I/R and whether long non-coding RNAs (lncRNAs) are involved in IFN-β-mediated myocardial injury remain unknown. This study identified that I/R significantly induced IFN-β expression in induced pluripotent stem cell-derived cardiomyocytes, and IFN-β further enhanced I/R-induced myocardial apoptosis. Furthermore, it was demonstrated that the lncRNA BRAF-activated non-coding RNA (BANCR) was highly expressed in cardiomyocytes, and BANCR-knockdown suppressed signal transducer and activator of transcription 1 (STAT1) phosphorylation and IFN-β-induced cardiomyocyte apoptosis. Furthermore, it was identified that BANCR specifically interacted with STAT1 to promote IFN-β-STAT1 signaling and enhanced the expression of pro-apoptotic interferon stimulated genes. Overall, the present study reports that lncRNA BANCR promotes IFN-β-mediated cardiomyocyte apoptosis following I/R injury by interacting with STAT1, suggesting lncRNA BANCR is involved in IFN-β-induced cardiomyocyte apoptosis.