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Abstract Due to their rapid and uncontrolled proliferation, cancer cells are characterized by overexpression of glutathione (GSH), which impairs reactive oxygen species (ROS)-based therapy and weakens the chemotherapeutic agent-induced toxification
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Metformin may suppress the key ferroptosis driver ACSL4 (which promotes toxic lipid biosynthesis) through AMPK pathway activation or reduce iron-dependent cellular damage by modulating iron metabolism-related proteins (e.g., downregulating transferrin receptor)
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