在肿瘤治疗中，蛋白酪氨酸激酶抑制剂（TKI）已被广泛使用。然而，TKI 的疗效明显受到耐药性的影响。因此，寻找有效的解决方案来克服 TKI 耐药性变得至关重要。活性氧（ROS）是一组高活性分子，在包括 TKI 靶向治疗在内的癌症靶向治疗中发挥着重要作用。在这篇综述中，我们重点关注肿瘤中 TKI 致死率的 ROS 相关机制以及调节 ROS 以逆转癌症中 TKI 耐药性的策略。在癌症 TKI 治疗过程中，ROS 水平经常升高，可能导致细胞器损伤和细胞死亡。对于 TKI 成功根除癌细胞至关重要。然而，值得注意的是，癌细胞可能会启动耐药途径来保护自己免受 ROS 诱导的损伤，从而导致 TKI 耐药。解决这一挑战需要阻断这些耐药途径，例如 NRF2-KEAP1 轴和保护性自噬，以促进细胞中 ROS 积累，从而使耐药癌细胞对 TKI 重新敏感。其他有效方法可诱导耐药细胞内产生 ROS，并提供外源性 ROS 刺激。ROS 在 TKI 根除肿瘤细胞中发挥着关键作用。利用 ROS 的积累来克服 TKI 耐药性是一种有效且广泛适用的方法。© 2024。作者。

In tumor treatment, protein tyrosine kinase inhibitors (TKIs) have been extensively utilized. However, the efficacy of TKI is significantly compromised by drug resistance. Consequently, finding an effective solution to overcome TKI resistance becomes crucial. Reactive oxygen species (ROS) are a group of highly active molecules that play important roles in targeted cancer therapy including TKI targeted therapy. In this review, we concentrate on the ROS-associated mechanisms of TKI lethality in tumors and strategies for regulating ROS to reverse TKI resistance in cancer.Elevated ROS levels often manifest during TKI therapy in cancers, potentially causing organelle damage and cell death, which are critical to the success of TKIs in eradicating cancer cells. However, it is noteworthy that cancer cells might initiate resistance pathways to shield themselves from ROS-induced damage, leading to TKI resistance. Addressing this challenge involves blocking these resistance pathways, for instance, the NRF2-KEAP1 axis and protective autophagy, to promote ROS accumulation in cells, thereby resensitizing drug-resistant cancer cells to TKIs. Additional effective approaches inducing ROS generation within drug-resistant cells and providing exogenous ROS stimulation.ROS play pivotal roles in the eradication of tumor cells by TKI. Harnessing the accumulation of ROS to overcome TKI resistance is an effective and widely applicable approach.© 2024. The Author(s).