Objective:To explore the mechanism and new therapeutic targets of anthracycline-induced cardiotox-icity.Methods:A total of 106 cases of breast cancer patients were divided into cardiac dysfunction group and control group based on echocardiography to identify cancer therapeutics-related cardiac functional impairment.Differentially expressed miRNAs between the two groups were screened out by high-throughput microarray tech-nology.The model of H9C2 myocardial cell damage induced by anthracyclines was constructed in vitro,and the role of miR-25a-5p in the H9C2 myocardial cell damage induced by anthracyclines was observed by regulating the expression of miR-25a-5p.Results:Cancer therapeutics-related cardiac dysfunction occurred in 9 breast can-cer patients,and a total of 9 differentially expressed miRNAs were identified between the two groups.Eight of these miRNAs were further validatedin vitromodel,especially miR-25a-5p.Up-regulation of miR-25a-5p could further aggravate the anthracycline-induced oxidative damage in myocardial cells.Conclusion:The miR-25a-5p aggravates anthracycline-induced myocardial damage and may be a new biomarker and therapeutic target.
关键词
乳腺癌/蒽环类药物/肿瘤治疗相关心功能障碍/miR-25a-5p
Key words
breast cancer/anthracycline/cancer therapeutics-related cardiac dysfunction/miR-25a-5p
维普
万方数据