Ferroptosis is a novel form of iron‑dependent programmed apoptosis, characterized by dysregulated iron metabolism, impaired antioxidant defense systems and accumulation of lipid peroxidation products. Nasopharyngeal carcinoma (NPC) cells exhibit marked susceptibility to ferroptosis, and its induction can effectively suppress tumor progression, offering a potential therapeutic strategy for NPC. At the molecular level, ferroptosis‑related genes [such as Solute Carrier Family 7 Member 11 (SLC7A11), Glutamate‑Cysteine Ligase Modifier Subunit (GCLM) and Glutamate‑Cysteine Ligase Catalytic Subunit (GCLC)] are notably upregulated in NPC tissues compared with normal tissues, and their overexpression associates with poor patient prognosis, suggesting their utility as diagnostic or prognostic biomarkers. The present review systematically summarizes the molecular mechanisms of ferroptosis, elucidates its role in NPC pathogenesis and discusses ferroptosis‑targeted therapeutic approaches for NPC.
Keywords: Epstein‑Barr virus; ferroptosis; lipid peroxidation; nasopharyngeal carcinoma; regulatory mechanisms.