Abstract

Ferroptosis is defined as an iron-dependent, non-apoptotic programed cell death modality that occurs due to an imbalance of intracellular redox hemostasis. Recently, ferroptosis has attracted attention in cancer research and has been shown to play a role in numerous oncogenic pathways. Studies have revealed that increased levels of intracellular reactive oxygen species play critical roles in oncogenic processes such as tumorigenesis, angiogenesis, invasion, metastasis, and chemoresistance because of their role in ferroptotic cell death. Neuroblastoma is the most common extracranial solid tumor in children and represents 8-10% of all pediatric cancers and 1/3 of all malign diseases of infancy. As seen in all types of cancers, the development of chemoresistance seriously affects the success of neuroblastoma treatment. Tolerance to chemotherapy in neuroblastoma was associated with the induction of exogenous defense genes and reduction of ferroptosis susceptibility biomarkers. Therefore, ferroptosis is a potential druggable driver in cancer treatment. In this review, studies associated with ferroptosis and neuroblastoma to date were reviewed and literature data were assessed in terms of ferroptotic mechanisms in neuroblastoma and potential treatment targets.