{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T01:33:29Z","timestamp":1792460009698,"version":"4.5.0"},"reference-count":69,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T00:00:00Z","timestamp":1781654400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:p>\n                    Prostate cancer (PCa) is a leading malignancy, and progression to castration-resistant prostate cancer (CRPC) remains a central therapeutic challenge. Cuproptosis, a copper-dependent cell death mechanism first characterized in 2022, is triggered by copper binding to lipoylated tricarboxylic acid (TCA)-cycle proteins, inducing their aggregation, Fe-S cluster protein instability, and mitochondrial proteotoxic stress. This review critically evaluates the emerging but still heterogeneous evidence linking cuproptosis to PCa, explicitly distinguishing prostate cancer-specific data from pan-cancer,non-prostate, bioinformatic, and preclinical observations. We describe the core machinery, including ferredoxin 1 (FDX1), dihydrolipoamide acetyltransferase (DLAT), protein lipoylation enzymes, and copper transport\/chaperone systems, while emphasizing differences from apoptosis and ferroptosis. In PCa, altered copper homeostasis and mitochondrial metabolic rewiring provide a biologically plausible vulnerability, but current evidence does not yet establish cuproptosis as a validated clinical driver or therapeutic target. We therefore summarize cuproptosis-related gene expression profiles and prognostic models as hypothesis-generating biomarkers,\u00a0and provide a prostate cancer-specific evidence table that separates bioinformatic,\n                    <jats:italic>in vitro<\/jats:italic>\n                    ,\n                    <jats:italic>in vivo<\/jats:italic>\n                    , and clinical levels of support. We also review potential links with metabolic reprogramming, immune microenvironment modulation, PD-L1 regulation, androgen receptor signaling, PTEN\/PI3K pathway activity, epigenetic regulation, and crosstalk with ferroptosis. Therapeutically, copper ionophores such\u00a0as elesclomol and disulfiram\/copper, and copper-depleting approaches such as chelators, are discussed as investigational strategies rather than near-clinical solutions. Particular attention is given to toxicity, narrow therapeutic windows, negative or inconclusive clinical data, the absence of validated companion diagnostics in PCa, and the need for patient-selection biomarkers based on copper handling, FDX1\/lipoylation status, and mitochondrial dependency. Finally, we outline the experimental and translational studies required before cuproptosis-directed interventions can be rationally tested in advanced PCa.\n                  <\/jats:p>","DOI":"10.3389\/fonc.2026.1874772","type":"journal-article","created":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T04:48:07Z","timestamp":1781671687000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Cuproptosis and prostate cancer: from molecular mechanisms and microenvironment remodeling to precision therapy"],"prefix":"10.3389","volume":"16","author":[{"given":"Zhonghao","family":"Tang","sequence":"first","affiliation":[{"name":"Department of Urology, Affiliated Hospital of Jiangnan University","place":["Wuxi, Jiangsu, China"]},{"name":"Wuxi School of Medicine, Jiangnan University","place":["Wuxi, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Si","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Urology, Affiliated Hospital of Jiangnan University","place":["Wuxi, Jiangsu, China"]},{"name":"Wuxi School of Medicine, Jiangnan University","place":["Wuxi, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Urology, Affiliated Hospital of Jiangnan University","place":["Wuxi, Jiangsu, China"]},{"name":"Wuxi School of Medicine, Jiangnan University","place":["Wuxi, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anjie","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Urology, Affiliated Hospital of Jiangnan University","place":["Wuxi, Jiangsu, China"]},{"name":"Wuxi School of Medicine, Jiangnan University","place":["Wuxi, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongjie","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pathology, Affiliated Hospital of Jiangnan University","place":["Wuxi, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Urology, Affiliated Hospital of Jiangnan University","place":["Wuxi, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanyuan","family":"Mi","sequence":"additional","affiliation":[{"name":"Department of Urology, Affiliated Hospital of Jiangnan University","place":["Wuxi, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,6,17]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/aja.2011.122","article-title":"What controls PTEN and what it controls (in prostate 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