ArticleRedox biology2022
BRCA1 haploinsufficiency promotes chromosomal amplification under Fenton reaction-based carcinogenesis through ferroptosis-resistance.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Iron-catalyzed oxidative stress reveals an exposome-related ferroptosis-resistant karyomegalic niche in BRCA1-linked renal carcinogenesis.Redox biology · 2026Article
- Choline metabolism drives metastasis in BRCA1-deficient ovarian cancers by activating FAM3C.Nature communications · 2026Article
- Genetic mutations governing ferroptosis sensitivity and resistance: a precision approach to cancer therapy.Cell death & disease · 2026Review
- Ferroptosis in renal cell carcinoma: integrative multi-omics insights and therapeutic perspectives.International journal of surgery (London, England) · 2026Article
- The role of ferroptosis in renal cell carcinoma: molecular mechanisms and therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Regulated cell death in cancer: Mechanisms, crosstalk, and opportunities for therapy.Cancer letters · 2025Review
- Acute kidney injury and iron metabolism: A narrative review focusing on pathophysiology and therapy.Smart molecules : open access · 2025Review
- Ferroptosis and cancer: when iron turns against tumors.Cellular and molecular life sciences : CMLS · 2025Review
- Susceptibility of Brca1Cancer science · 2025Article
- Exosome-mediated effects of BRCA1 on cardiovascular artery disease.Cell biology and toxicology · 2025Article
- Decoding the molecular enigma behind asbestos and fibrous nanomaterial-induced carcinogenesis.Journal of occupational health · 2025Review
- GPX4 and FSP1 Expression in Lung Adenocarcinoma: Prognostic Implications and Ferroptosis-Based Therapeutic Strategies.Cancers · 2024Article
- MJournal of nanobiotechnology · 2024Article
- Expression and Localization of Ferritin-Heavy Chain Predicts Recurrence for Breast Cancer Patients with aCancers · 2023Article
- Knockdown of SLC39A14 inhibits glioma progression by promoting erastin-induced ferroptosis SLC39A14 knockdown inhibits glioma progression.BMC cancer · 2023Article
- BRCA1 haploinsufficiency impairs iron metabolism to promote chrysotile-induced mesothelioma via ferroptosis resistance.Cancer science · 2023Article
- Environmental impact on carcinogenesis under BRCA1 haploinsufficiency.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Review
- Mitochondrial Iron Metabolism: The Crucial Actors in Diseases.Molecules (Basel, Switzerland) · 2022Review
- Brca1Cancer science · 2022Article
- Iron as spirit of life to share under monopoly.Journal of clinical biochemistry and nutrition · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Germline-mutation in BRCA1 tumor suppressor gene is an established risk for carcinogenesis not only in females but also in males. Deficiency in the repair of DNA double-strand breaks is hypothesized as a responsible mechanism for carcinogenesis. However, supporting data is insufficient both in the mutation spectra of cancers in the patients with BRCA1 germline-mutation and in murine knockout/knock-in models of Brca1 haploinsufficiency. Furthermore, information on the driving force toward carcinogenesis in BRCA1 mutation carriers is lacking. Here we applied Fenton reaction-based renal carcinogenesis to a rat heterozygously knockout model of BRCA1 haploinsufficiency (mutant [MUT] model; L63X/+). Rat MUT model revealed significant promotion of renal cell carcinoma (RCC) induced by ferric nitrilotriacetate (Fe-NTA). Array-based comparative genome hybridization of the RCCs identified significant increase in chromosomal amplification, syntenic to those in breast cancers of BRCA1 mutation carriers, including c-Myc, in comparison to those in the wild-type. Subacute-phase analysis of the kidney after repeated Fe-NTA treatment in the MUT model revealed dysregulated iron metabolism with mitochondrial malfunction assessed by expression microarray and electron microscopy, leading to renal tubular proliferation with iron overload. In conclusion, we for the first time demonstrate that biallelic wild-type BRCA1 provides more robust protection for mitochondrial metabolism under iron-catalyzed oxidative stress, preventing the emergence of neoplastic cells with chromosomal amplification. Our results suggest that oxidative stress via excess iron is a major driving force for carcinogenesis in BRCA1 haploinsufficiency, which can be a target for cancer prevention and therapeutics.
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