Crosstalk between the cell cycle and ferroptosis in tumor cells
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Updated: Nov 1, 2026

Revealing the Ferroptotic Phenotype of Medulloblastoma
Published on: March 15, 2024
Zongyao Zheng1, Xu Lin2, Xiang Wang3
1Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou 310006, China.
Abstract:
Cell-cycle regulation shapes ferroptosis through its influences on lipid metabolism, antioxidant defenses, and stress signaling. This review examines how p53, retinoblastoma protein, cyclin-dependent kinases, and DNA damage checkpoints influence ferroptosis in cancer. We reconcile the occurrence of both sensitization and resistance following cell cycle arrest by considering cellular state, arrest duration, lipid storage, redox status, and alternative defense pathways. Drug-tolerant persister cells are distinguished from other slowly proliferating cell populations. Proposed combination treatments remain preclinical, with translation constrained by pharmacokinetics, normal tissue toxicity, tumor heterogeneity, delivery, and unvalidated biomarkers. Functional metabolic assessment is therefore needed alongside cell cycle measurements to guide the future development of therapies that target the cell cycle and ferroptosis {AuQ: Edit OK?}.
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