Targeting ferroptosis to treat colorectal cancer

Ferroptosis has emerged as a promising target for colorectal cancer (CRC) treatment. Although disrupting glutathione metabolism is the primary strategy for ferropto-sis induction, additional key path-ways link ferroptosis to CRC pathogenesis. Here, we discuss arachidonic acid (AA), energy me-tabolism, AMP-activated protein ki-nase (AMPK), phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamy-cin (mTOR), and Hippo signaling, summarize key findings, and pro-pose new conceptual avenues for CRC treatment.