癌细胞的致癌基因诱导过度增殖，同时伴随着DNA复制压力，代谢压力和氧化应答等不同形式的压力。过度积累的活性氧自由基(ROS)在肿瘤进程中扮演了至关重要且矛盾的作用。ROS支配了大量的细胞信号通路，促进了肿瘤细胞的恶性转化。同时，肿瘤细胞内的氧化负担迫使其增强抗氧化能力以减轻其造成的伤害。癌细胞对氧化应答的依赖和对铁的需求增加也影响了镁死的敏感性。靶向氧化还原平衡和镁死以克服肿瘤治疗中的耐药性已成为一项魅力十足的研究课题。然而，致癌信号在氧化还原调节和镁死中的作用还没有被全面讨论。在此综述中，我们总结了关于癌症生物学背景下氧化还原平衡和镁死相互作用的当前知识。我们强调了致癌信号在氧化还原平衡和镁死调节中的意义，并概述了针对肿瘤治疗中氧化应答和镁死的策略。本文受版权保护，所有权利均属于原作者。

Oncogene-induced hyper-proliferation in cancer cells is accompanied by the onset of different stresses, including DNA-replication stress, metabolic stress and oxidative stress. Excessive accumulation of reactive oxygen species (ROS) plays a pivotal and contradictory role in tumor progression. ROS dictates a multitude of cell signaling pathways to facilitate the malignant transformation of tumor cells. In the meantime, oxidative burden in tumor cells mandates reinforcing antioxidant capacity to mitigate detrimental damages. The addiction to oxidative stress and increased iron demands in cancer cells also impinges on the sensitivity of ferroptosis. Targeting redox homeostasis and ferroptosis to overcome drug resistance in cancer treatment has become an attractive research topic. However, the roles of oncogenic signaling in redox regulation and ferroptosis have not been comprehensively discussed. In this review, we summarize current knowledge regarding the interplay between redox regulation and ferroptosis in the context of cancer biology. We emphasize the implication of oncogenic signaling in redox homeostasis and ferroptosis regulation. We also provide an overview of strategies targeting oxidative stress and ferroptosis in cancer treatment. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.