Ferroptosis: An emerging strategy for managing epithelial ovarian cancer - 17/05/25
, J. Fafián-Labora a, ⁎ Abstract |
Ferroptosis is a regulated form of cell death characterised by iron-dependent lipid peroxidation, a process intricately linked to cellular redox homeostasis. This form of cell death is induced by the accumulation of intracellular iron and the subsequent generation of reactive oxygen species (ROS), which leads to lipid peroxidation and ultimately cell death. Ferroptosis is distinct from traditional forms of cell death, such as apoptosis, and holds significant therapeutic potential, particularly in cancers harboring rat sarcoma virus (RAS) mutations, such as epithelial ovarian cancer (EOC). EOC is notoriously resistant to conventional therapies and is associated with a poor prognosis. In this review, we examine recent progress in the understanding of ferroptosis, with a particular focus on its redox biology and the complex regulatory networks involved. We also propose a novel classification system for ferroptosis modulators, grouping them into six categories (I, II, III, IV, V and VI) based on their mechanisms of action and their roles in modulating cellular redox status. By refining these categories, we aim to provide deeper insights into the role of ferroptosis in cancer biology, especially in EOC, and to identify potential therapeutic avenues. We propose that further investigation of ferroptosis in the context of redox biology could reveal novel biomarkers and therapeutic targets, offering promising strategies to overcome resistance mechanisms and improve clinical outcomes for patients with EOC and other treatment-resistant cancers.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | Ferroptosis, an iron-dependent cell death via lipid peroxidation, offers promise for treating EOC and overcoming therapy resistance. |
• | EOC cells show iron imbalance and oxidative stress, making them ferroptosis-sensitive, targeting this may improve cisplatin response. |
• | Key ferroptosis regulators like cyst(e)ine/GSH/GPX4 and NAD(P)H/FSP1/CoQ10 pathways offer targets for therapeutic intervention. |
• | Ferroptosis inducers and inhibitors can selectively manipulate this cell death pathway, paving the way for targeted cancer treatments. |
• | The combination of ferroptosis-inducing compounds with conventional therapies, identification of biomarkers, and use of extracellular vesicles for drug delivery hold potential to significantly improve EOC patient outcomes. |
Abbreviations : 4-HNE, 4EBP, ACSL3, ACSL4, AIF, ALOX15, AMPK, APGS, ApoER2, ATP, BCS, BH 2 , BH 4 , BI-1356, BSO, C107, C148, Ca 2 + , CD44, CoQ 10 , COX17, Cu 2+ , D-PUFAs, DHA, DHO, DHODH, DMT1, DPC, DPP4, EGFR, EOC, ER, EVs, FBXL5, Fe-S, Fe 2+ , Fe 3+ , FMN, FPN/FPN1, FSP1, FTH, FTL, GALNT14, GCH1, GPX4, GPXs, GS, GSH, GSSG, GTP, H2Bub1, H 2 O 2 , HERC2, HERPUD1, HIF-1α, HMGB1, HMOX1, HUVECs, IKE, IMCA, IONP-GA/PAA, IRP1/2, ITPR, LAF-237, LOX, LPCAT, LRP8, MDA, MS4A15, mTOR, mTORC1, mTORC2, MUFAs, N/A, NADH, NADP + , NADPH, NCOA4/NCO4, NDGA, NDH-2, NEAT1, Nedd4, NF2, NPs, NRF2, oxPLs, p53, PDAC, Prdx I/II, PUFA-CoA, PUFA-ePLs, PUFA-GP, PUFA-OH, PUFA-OOH, PUFAs/ PUFA, PUFA-PL, Rag, RAS, RNA, ROS, RSL, RSL3, RTA, SCD1, SEPP1, SLC30, SLC39, SLC7A11, SYR 322, TAX1BP1, TFEB, TFRC, TRF, UMP, UV, VAMP8, VDAC2/3, VDACs, VK/VE, VKH/VEH, YAP, ZEB1, ZIP1, ZIP7, Zn, ZnO, ZnT
Keywords : Ferroptosis, Epithelial ovarian cancer, Redox biology
Plan
Vol 187
Article 118065- juin 2025 Retour au numéro
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