Abstract
Ferroptosis is an atypical form of regulated cell death, which is different from apoptosis, necrosis, pyroptosis, and autophagy. Ferroptosis is characterized by iron-dependent oxidative destruction of cellular membranes following the antioxidant system's failure. The sensitivity of ferroptosis is tightly regulated by a series of biological processes, the metabolism of iron, amino acids, and polyunsaturated fatty acids, and the interaction of glutathione (GSH), NADPH, coenzyme Q10 (CoQ10), and phospholipids. Elevated oxidative stress (ROS) level is a hallmark of cancer, and ferroptosis serves as a link between nutrition metabolism and redox biology. Targeting ferroptosis may be an effective and selective way for cancer therapy. The underlying molecular mechanism of ferroptosis occurrence is still not enough. This review will briefly summarize the process of ferroptosis and introduce critical molecules in the ferroptotic cascade. Furthermore, we reviewed the occurrence and regulation of reduction-oxidation (redox) for ferroptosis in cancer metabolism. The role of the tumor suppressor and the epigenetic regulator in tumor cell ferroptosis will also be described. Finally, old drugs that can be repurposed to induce ferroptosis will be characterized, aiming for drug repurposing and novel drug combinations for cancer therapy more efficiently and economically.
Highlights
Ferroptosis is an atypical form of programed cell death first proposed by Dixon et al in 2012 [1] and is different from apoptosis, pyroptosis, autophagy, or the other types of cell death in morphology, biochemistry, and genetics
We summarized the basic regulation in oxidative-induced ferroptosis and its latest advances firstly, and the old drugs which can be repurposed for proferroptotic anticancer therapy has been described, which is aimed at expanding the new indications for existing drugs and alleviating the shortage of medicine for drug-resistant patients [13]
Substantial progress has been made about how tumor metabolism and oncogenic mutation regulate the sensitivity of ferroptosis, the extent to which the mutation profile affects the sensitivity to ferroptosis is still unclear
Summary
Ferroptosis is an atypical form of programed cell death first proposed by Dixon et al in 2012 [1] and is different from apoptosis, pyroptosis, autophagy, or the other types of cell death in morphology, biochemistry, and genetics. An emerging evidence shows that oncogenes and tumor suppressors’ change both have essential impacts on tumor cell ferroptosis regulation. The regulation of antioxidant homeostasis is essential in maintaining cancer cell survival and normal cellular function. An emerging evidence shows that the ability to adapt to aberrant metabolism and escape from immunosurveillance is essential for tumor cell survival [12]. Targeting the “cart” (metabolism, immune) rather than the “horse” (oncogenes and tumor suppressors) may provide a new horizon for cancer therapy efficiently and selectively. Ferroptosis can be a powerful tool to develop a new strategy by amplifying oxidative stress or inhibiting antioxidant regulators in tumor cells. We summarized the basic regulation in oxidative-induced ferroptosis and its latest advances firstly, and the old drugs which can be repurposed for proferroptotic anticancer therapy has been described, which is aimed at expanding the new indications for existing drugs and alleviating the shortage of medicine for drug-resistant patients [13]
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