Ferroptosis is a novel form of regulated cellular necrosis that plays a critical role in promoting cancer progression and developing drug resistance. The main characteristic of ferroptosis is iron‑dependent lipid peroxidation caused by excess intracellular levels of reactive oxygen species. CUGBP ELAV‑like family number 2 (CELF2) is an RNA‑binding protein that is downregulated in various types of cancer and is associated with poor patient prognoses. CELF2 can directly bind mRNA to a variety of ferroptosis control factors; however, direct evidence of the regulatory role of CELF2 in ferroptosis is currently limited. The aim of the present review was to summarise the findings of previous studies on CELF2 and its role in regulating cellular redox homeostasis. The present review may provide insight into the possible mechanisms through which CELF2 affects ferroptosis and to provide recommendations for future studies.
Keywords: CUGBP ELAV‑like family number 2; MAPK signalling pathway; PI3K/AKT signalling pathway; Wnt/β‑catenin pathway; autophagy; endoplasmic‑reticulum‑associated protein degradation; ferroptosis.