Abstract
Abstract Ferroptosis is an iron-dependent mode of programmed cell death characterized by Reactive Oxygen Species (ROS) accumulation lipid peroxidation and glutathione depletion. It is a novel form of cell death different from apoptosis and necrosis. Because of its unique mode of cell death, it has attracted a large number of research reports from the oncology community. Changes in iron ions and accumulation of lipid peroxides have confirmed the correlation between ferroptosis and tumors, and thus ferroptosis can be considered to have a great oncological therapeutic potential. This paper brings to light the significance of metabolic pathways and key genes like System Xc-/Glutathione Peroxidase 4 (GPX4), Membrane-bound O-acyltransferases 1 (MBOAT1) and Membrane-bound O-acyltransferases 2 (MBOAT2) in modulating ferroptosis in cancer cells. The susceptibility of cancer cells to ferroptosis, influenced by their high levels of reactive oxygen species and specific mutation profiles, is analyzed, suggesting new avenues for enhancing the effectiveness of established cancer treatments. In this review, we address the current understanding of ferroptosis induction and ferroptosis defense mechanisms, briefly describe the role and mechanisms of ferroptosis in tumor suppression, and discuss therapeutic strategies for targeting ferroptosis caused by tumors.
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