临床应用化疗治疗肺癌受制于副作用，特别是心脏毒性，其机制尚不清楚。本研究评估特定miRNA在肺癌化疗所致心脏毒性中的生物标志物潜力。我们采用两种肺腺癌细胞系（Calu6和H1792）和心室正常人心脏成纤维细胞（NHCF-V）进行单独和共培养实验。使用100 µM卡铂和1 µM长春瑞滨剂量进行功能性测试。对于单独培养和共培养的细胞和分子水平，在治疗后48小时评估卡铂和长春瑞滨的单独和联合效应。分析了癌症治疗中通过调节心脏毒性的miR-205-5p，miR-21-5p和miR-30a-5p。长春瑞滨和卡铂治疗在肺癌细胞和心脏成纤维细胞中促进了凋亡和自噬的程度大于对照组。Western blot分析显示BCL2和p53蛋白上调。通过qRT-PCR，我们研究了共培养的心肌细胞和肺癌细胞中miR-21-5p、miR-30c-5p和miR-205-5p的表达动态，揭示了长春瑞滨和卡铂治疗导致的miRNA模式改变。我们的发现强调了化疗、miRNA调控和心脏毒性之间的复杂关系，突出了肺癌治疗决策中心脏健康的重要性。

Clinical application of chemotherapy in lung cancer is constrained by side effects, notably cardiotoxicity, the mechanisms of which remain elusive. This study assessed the potential of specific miRNAs as biomarkers for chemotherapy-induced cardiotoxicity in lung cancer. We employed two lung adenocarcinoma cell lines (Calu6 and H1792) and ventricular normal human cardiac fibroblasts (NHCF-V) in single and co-culture experiments. Functional tests were conducted using 100 µM carboplatin and 1µM vinorelbine doses. The effects of carboplatin and vinorelbine, both individually and in combination, were evaluated at cellular and molecular levels 48h post-therapy for both mono- and co-cultures. miR-205-5p, miR-21-5p, and miR-30a-5p, modulated by anticancer treatments and influencing cardiotoxicity, were analyzed. Vinorelbine and carboplatin treatment promoted apoptosis and autophagy in lung cancer cells and cardiac fibroblasts more than in controls. Western blot analyses revealed BCL2 and p53 protein upregulation. Using qRT-PCR, we investigated the expression dynamics of miR-21-5p, miR-30c-5p, and miR-205-5p in co-cultured cardiomyocytes and lung cancer cells, revealing altered miRNA patterns from vinorelbine and carboplatin treatment. Our findings underscore the intricate relationship between chemotherapy, miRNA regulation, and cardiotoxicity, highlighting the importance of cardiac health in lung cancer treatment decisions.