LncRNA NKILA Promotes Cardiomyocytes Apoptosis by Targeting miR22-3p-TXNIP Signal Axis to Inhibit Proliferation, Migration, and Invasion of Cardiomyocytes under High Glucose-Induced Condition

This study aims to investigate the molecular mechanism of LncRNA NKILA underlying promoting cardiomyocytes apoptosis and relevant diabetic cardiomyopathy. We utilized high concentration of glucose to induce human cardiomyocytes cell line AC16 to imitate diabetic cardiomyopathy. an‎d then, we performed high-throughput big data analysis, RT-PCR, and western blot assays to evaluate the expression levels of associated mRNA and protein. Cell apoptosis was tested by Annexin V-FITC. The proliferation, migration, and invasion of AC16 cells were examined by CCK8 assay, colony formation assay, EdU assay, wound healing test, and transwell chamber assay. We utilized statistical analysis and luciferase activity assay to analyze the interaction of relevant genes. LncRNA NKILA was highly expressed in AC16 cells induced by high glucose and inhibited AC16 cell proliferation, migration, and invasion by inducing cell apoptosis. Luciferase activity assay demonstrated that LncRNA NKILA binds to miR22-3p. The influence of LncRNA NKILA on AC16 cell proliferation, migration, and invasion could be reversed by miR22-3p. Luciferase activity assay demonstrated that TXNIP was a target of miR-22-3p in AC16 cells, and all the effects of TXNIP on AC16 cell proliferation, migration, and invasion could be abolished by miR22-3p. These results provided comprehensive data about a novel molecular mechanism of LncRNA NKILA promoting cardiomyocytes apoptosis: LncRNA NKILA performed its function in AC16 cells under high glucose-induced condition by targeting mir-22-3p-TXNIP signal axis, which indicated that LncRNA NKILA may play a crucial role in diabetic cardiomyopathy.