Reactive oxygen species regulation of ferroptosis, autophagy, apoptosis, and immunogenic cell death in cancer
TL;DR
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.
Abstract
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.