The DOI matches its Crossref record; 120 of the 121 references it cites were found in a registry or an index.
Iron and cancer: recent insights
Open accessAbstract
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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“cancer cells have a high demand for easily accessible labile Fe2+ for their survival and growth.”
From Targeting cancer vulnerabilities with high-dose vitamin C (2019) · cites this paper as [23]
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“Nuclear receptor coactivator 4 (NCOA4)‐mediated ferritino-phagy delivers ferritin to lysosomes, where iron is released, and the labile iron pool is increased (Chen et al. 2021; Manz et al. 2016; Zeng et al. 2023).”
Procopciuc, L. M., Hangan, A. C., & Lucaciu, R. L. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27209244
“This iron-dependent phenotype, sometimes referred to as iron addiction, supports malignant growth but carries an intrinsic risk because excess redox-active Fe 2+ can promote ROS generation and lipid peroxidation [54,55].”
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Metadata
- Authors
- Manz, D. H., Blanchette, N. L., Paul, B. T., Torti, F. M., & Torti, S. V.
- Affiliations
- Department of Molecular Biology and Biophysics
- UConn Health (US)
- Corresponding author
- Torti, Suzy V.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2016-02-18
- Volume
- 1368
- Issue
- 1
- Pages
- 149-161
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC4870095
- OpenAlex
- W2275201610
- Cited by
- 507
- References
- 121
- Citations by year
- 2026: 24 · 2025: 49 · 2024: 69 · 2023: 78 · 2022: 66 · 2021: 77 · 2020: 46 · 2019: 43 · 2018: 31 · 2017: 14 · 2016: 10
- FWCI
- 4.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- S.V.T (CA188025)
- F.M.T (CA171101)
- D.H.M. (DE021989)
- U.S. National Institutes of Health
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- iron metabolism, cancer, ferroptosis, ferroportin, hepcidin, iron efflux, reactive oxygen species, glutathione depletion, GPX4, ferritinophagy, ferritin degradation, tumor microenvironment, epigenetic regulation, microRNA, DNA methylation, histone acetylation, cancer therapy
- MeSH terms
- Ferroportin, Animals, Humans, Iron, Neoplasms, Reactive Oxygen Species, Iron Overload, Cation Transport Proteins
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