LncRNA KCNQ1OT1 contributes to hydrogen peroxide‐induced apoptosis, inflammation, and oxidative stress of cardiomyocytes via miR‐130a‐3p/ZNF791 axis

It has been reported that long noncoding RNA (lncRNA) KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) played an important role in myocardial infarction (MI). However, the regulatory network behind KCNQ1OT1 in MI is largely unknown. Quantitative real time polymerase chain reaction (qRT‐PCR) was applied to detect the enrichment of KCNQ1OT1, microRNA‐130a‐3p (miR‐130a‐3p) and zinc finger 791 (ZNF791). The viability and apoptosis of AC16 cells were measured by (4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay and flow cytometry. Enzyme‐linked immunosorbent assay (ELISA) was conducted to assess the inflammation and oxidative stress status of AC16 cells. The targeted relationship between miR‐130a‐3p and KCNQ1OT1 or ZNF791 was predicted by StarBase bioinformatic database, and dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay were carried out to verify these predictions. Hydrogen peroxide (H2O2) stimulation caused a significant upregulation in the expression of KCNQ1OT1, while the level of miR‐130a‐3p showed an opposite phenomenon. KCNQ1OT1 was a crucial downstream component in H2O2‐mediated toxic effects, and KCNQ1OT1 accelerated H2O2‐induced toxic effects in AC16 cells. KCNQ1OT1 could sponge miR‐130a‐3p and down‐regulate its expression. MiR‐130a‐3p exerted opposite effects to KCNQ1OT1, and the depletion of miR‐130a‐3p attenuated the protective effects of KCNQ1OT1 intervention on AC16 cells exposed to H2O2. MiR‐130a‐3p could bind to ZNF791, and ZNF791 served as the target of miR‐130a‐3p to promote H2O2‐induced injury of AC16 cells. ZNF791 was modulated by KCNQ1OT1/miR‐130a‐3p signaling in H2O2‐treated AC16 cells. In all, lncRNA KCNQ1OT1 deteriorated H2O2‐mediated injury in cardiomyocytes through upregulating ZNF791 via serving as a molecular sponge for miR‐130a‐3p.