Journal
COOLEY'S ANEMIA
Volume 1368, Issue -, Pages 149-161Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.13008
Keywords
iron; cancer; ferroptosis; ferritinophagy
Categories
Funding
- NCI NIH HHS [R01 CA171101, R01 CA188025] Funding Source: Medline
- NIDCR NIH HHS [T90 DE021989] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA188025, R01CA171101] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [T90DE021989] Funding Source: NIH RePORTER
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Iron is an essential dietary element. However, the ability of iron to cycle between oxidized and reduced forms also renders it capable of contributing to free radical formation, which can have deleterious effects, including promutagenic effects that can potentiate tumor formation. Dysregulation of iron metabolism can increase cancer risk and promote tumor growth. Cancer cells exhibit an enhanced dependence on iron relative to their normal counterparts, a phenomenon we have termed iron addiction. Work conducted in the past few years has revealed new cellular processes and mechanisms that deepen our understanding of the link between iron and cancer. Control of iron efflux through the combined action of ferroportin, an iron efflux pump, and its regulator hepcidin appears to play an important role in tumorigenesis. Ferroptosis is a form of iron-dependent cell death involving the production of reactive oxygen species. Specific mechanisms involved in ferroptosis, including depletion of glutathione and inhibition of glutathione peroxidase 4, have been uncovered. Ferritinophagy is a newly identified mechanism for degradation of the iron storage protein ferritin. Perturbations of mechanisms that control transcripts encoding proteins that regulate iron have been observed in cancer cells, including differences in miRNA, methylation, and acetylation. These new insights may ultimately provide new therapeutic opportunities for treating cancer.
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