Han Xiao, Liu Kun, Gao Fumin, Yang Mingjun, Wang Fei
Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, Jiangsu, 226001, China.
Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Open Med (Wars). 2023 Jul 25;18(1):20230754. doi: 10.1515/med-2023-0754. eCollection 2023.
Irreversible cardiomyopathy was caused by the therapeutic of anthracyclines in the chemotherapy of cancers. The cell apoptosis and autophagy were induced by anthracyclines in AC16 cells. MiR-223-3p ascends in anthracycline-treated AC16, but the expression of nuclear factor I-A (NFIA) was specifically down-regulated. However, the underlying molecular mechanism between NFIA and miR-223-3p is unclear now in AC16 cells. In our research, NFIA expression was dampened in AC16 cells by miR-223-3p mimics. Additionally, miR-223-3p knockdown hindered the apoptosis and autophagy in anthracycline-treated AC16. Furthermore, NFIA was predicted and verified as a miR-223-3p's downstream target and rescued the functions of miR-223-3p. These findings illustrated that miR-223-3p advances anthracycline-stimulated cardiomyocyte damage progression by targeting NFIA, implying the promising therapeutic function of miR-223-3p on cardiomyocyte damage in cancer patients.
不可逆性心肌病是由癌症化疗中蒽环类药物的治疗引起的。蒽环类药物在AC16细胞中诱导细胞凋亡和自噬。在经蒽环类药物处理的AC16细胞中，miR-223-3p升高，但核因子I-A（NFIA）的表达特异性下调。然而，目前在AC16细胞中，NFIA与miR-223-3p之间潜在的分子机制尚不清楚。在我们的研究中，miR-223-3p模拟物使AC16细胞中的NFIA表达降低。此外，敲低miR-223-3p可抑制经蒽环类药物处理的AC16细胞中的凋亡和自噬。此外，NFIA被预测并验证为miR-223-3p的下游靶点，并挽救了miR-223-3p的功能。这些发现表明，miR-223-3p通过靶向NFIA促进蒽环类药物刺激的心肌细胞损伤进展，这意味着miR-223-3p对癌症患者心肌细胞损伤具有潜在的治疗作用。
