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Reactive oxygen species regulation of ferroptosis; autophagy; apoptosis; and immunogenic cell death in cancer
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DOI：10.3389/fphys.2026.1908766.png)
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Abstract
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Reactive oxygen species (ROS) are produced during metabolism through mitochondrial oxidative phosphorylation and NADPH oxidase activity. In cancer; ROS exhibit a paradoxical; concentration-dependent dual role. At low to moderate levels; ROS promote tumor cell survival; EMT; and metastasis; and at high levels; ROS overwhelm antioxidant defenses and induce regulated cell death (RCD); ferroptosis; autophagy; apoptosis; and immunogenic cell death (ICD) have emerged as significant ROS-dependent targets in cancer therapy. This review summarizes recent advances in ROS-controlled ferroptosis; autophagy; apoptosis; and ICD; emphasizing the roles of the GPX4/SLC7A11; AMPK/mTORC1/Beclin-1; Bcl-2/Bax/cytochrome c; and damage-associated molecular pattern (DAMP)-mediated signal cascade; their crosstalk; and therapeutic potential for targeting tumor redox vulnerabilities.
Keywords:
ferroptosis
apoptosis
autophagy
cancer therapy
ROS
ICD
Journal
IF:
3.4
Papers:
1.9W
Citations:
6.2W
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Cited Papers