{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T04:55:04Z","timestamp":1790571304369,"version":"4.1.0"},"reference-count":110,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T00:00:00Z","timestamp":1790467200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T00:00:00Z","timestamp":1790467200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Asia-Pac J Clncl Oncology"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Breast cancer remains a significant clinical challenge, particularly in triple\u2011negative breast cancer (TNBC), in which therapeutic resistance limits treatment efficacy. Ferroptosis, an iron\u2010dependent form of regulated cell death driven by lipid peroxidation, has emerged as a promising strategy to overcome resistance in breast cancer. Among the principal nodulators of ferroptosis, NRF2 functions as a central antioxidant transcription factor that suppresses ferroptotic death by promoting glutathione metabolism and cystine uptake via SLC7A11\/system Xc\u2212, while also supporting GPX4\u2010dependent lipid peroxide detoxification and iron\u2010sequestering defenses such as FTH1\/FTL. In breast cancer, aberrant NRF2 activation supports tumor progression, survival, stemness, immune evasion, and resistance to chemotherapy, radiotherapy, and targeted therapies. This review summarizes the molecular mechanisms by which NRF2 regulates ferroptosis, including KEAP1\u2013NRF2 signaling, metabolic rewiring, iron homeostasis, lipid remodeling, and crosstalk with p53 and other stress\u2010response pathways. We also highlight key regulators such as PRMT5, NUP62, NR5A2\/NCOA3, miR\u2010141\u20103p, DHODH, and ACSL4\/ALOX enzymes that shape ferroptosis sensitivity. Furthermore, the review discusses emerging therapeutic approaches aimed at restoring ferroptotic vulnerability, including direct NRF2 inhibitors, natural products, metal\u2010based compounds, repurposed drugs, and nanotechnology\u2010enabled delivery systems. TNBC is specifically reliant on NRF2\u2010driven antioxidant defenses to maintain redox homeostasis and resist ferroptotic stress, supporting its prioritization as a target population for NRF2\u2013ferroptosis\u2010based therapeutic methods. Collectively, targeting the NRF2\u2013ferroptosis axis offers a compelling avenue for improving breast cancer treatment, especially in resistant and aggressive subtypes such as TNBC.<\/jats:p>","DOI":"10.1111\/ajco.70195","type":"journal-article","created":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T03:56:46Z","timestamp":1790567806000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["NRF2\u2010Regulated Ferroptosis in Breast Cancer: Mechanisms, Resistance, and Therapeutic Opportunities"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6156-9063","authenticated-orcid":false,"given":"Suleiman Ibrahim","family":"Mohammad","sequence":"first","affiliation":[{"name":"Department of Business Administration Business School Al al\u2010Bayt University  Mafraq Jordan"},{"name":"INTI International University 71800 Negeri Sembilan 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