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Cancer Related Molecular Mechanisms Research / Cancer, Hypoxia, and Metabolism / Ferroptosis and Cancer Prognosis · Journal article
Frontiers in Physiology · August 10, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review summarizing mechanistic knowledge of how reactive oxygen species control ferroptosis, autophagy, apoptosis, and immunogenic cell death in cancer via specific signaling cascades (GPX4/SLC7A11, AMPK/mTORC1/Beclin-1, Bcl-2/Bax/cytochrome c, and DAMP-mediated pathways). The work identifies therapeutic targets and crosstalk between pathways but does not report clinical trial data, animal studies, or empirical evidence of efficacy.
Journal article.
ROS exhibit concentration-dependent dual role: at low to moderate levels promote tumor survival and metastasis; at high levels overwhelm antioxidant defenses and induce regulated cell death. Four ROS-dependent regulated cell death pathways identified as significant cancer therapy targets: ferroptosis, autophagy, apoptosis, and immunogenic cell death. Key signaling cascades implicated: GPX4/SLC7A11, AMPK/mTORC1/Beclin-1, Bcl-2/Bax/cytochrome c, and damage-associated molecular pattern (DAMP)-mediated signal cascade.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
A narrative review synthesizing mechanistic pathways of ROS-dependent cell death in cancer, raising questions about therapeutic targeting rather than reporting empirical trial results.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
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.
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