fig1
Figure 1. Ferroptosis-related signaling pathways in cancer drug resistance. The signaling pathways that promote ferroptosis mainly include those related to the oxidant system, iron toxicity, and the production and peroxidation of PUFA-PLs, while the signaling pathways that inhibit ferroptosis primarily involve GPX-dependent and FSP1-dependent antioxidant signaling pathways, as well as those related to MUFA-PL synthesis. In cancer drug resistance, pro-ferroptosis key factors such as ACSL4 are downregulated, while anti-ferroptosis factors like GPX4, NRF2, FSP1, NFS1, and ACSL3 are upregulated. SLC3A2: Solute carrier family 3 member 2; SLC7A11: solute carrier family 7 member 11; GSH: glutathione; GSSG: oxidized glutathione; GPX4: glutathione peroxidase 4; CoQ: coenzyme Q; CoQH2: reduced coenzyme Q; FSP1: ferroptosis suppressor protein 1; VK: vitamin K; VKH2: reduced vitamin K; VKORC1L1: vitamin K epoxide reductase complex subunit 1-like 1; NRF2: nuclear factor E2-related factor 2; KEAP1: Kelch-like ECH-associated protein 1; KRAS: Kirsten rat sarcoma viral oncogene homolog; BRAF: B-Raf proto-oncogene; MYC: myelocytomatosis oncogene; LIP: labile iron pool; PLOOH: phospholipid hydroperoxides; NFS1: cysteine desulfurase; PUFA: polyunsaturated fatty acid; CoA: coenzyme A; ACSL4: acyl-CoA synthetase long-chain family member 4; PL: phospholipid; LPCAT3: lysophosphatidylcholine acyltransferase 3, incorporating fatty acids especially PUFAs into PLs; SFA: saturated fatty acid; MUFA: monounsaturated fatty acid; SCD1: stearoyl-CoA desaturase 1; ACSL3: acyl-CoA synthetase long-chain family member 3, activating MUFAs.
