[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-337333-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-337333-en":130},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","advances-in-ferroptosis-for-castration-resistant-prostate-cancer-treatment-novel-drug-targets-and-combination-therapy-strategies","Advances in ferroptosis for castration-resistant prostate cancer treatment: novel drug targets and combination therapy strategies","","Metastatic prostate cancer has poor survival and typically progresses to castration resistance, creating an urgent need for new targets and therapeutic strategies. This review summarizes ferroptosis mechanisms, its functional effects in castration-resistant prostate cancer, and its links to treatment response and prognosis. Ferroptosis regulators such as PI3K/AKT/mTOR and DECR1, along with inducers erastin, BSO, RSL3, and FIN56, are discussed. Radiation-induced anticancer effects, radiosensitizing GPX4 and SLC7A11 inhibition, and ferroptosis-related gene risk models are highlighted.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/advances-in-ferroptosis-for-castration-resistant-prostate-cancer-treatment-novel-drug-targets-and-combination-therapy-strategies/337333/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/advances-in-ferroptosis-for-castration-resistant-prostate-cancer-treatment-novel-drug-targets-and-combination-therapy-strategies/337333.png","ImageObject",300,407,{"name":42,"@type":43},"Ophelia","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-29","2026-09-21",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",8,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"Why is castration-resistant prostate cancer a major clinical challenge?","Question",{"text":63,"@type":64},"Metastatic prostate cancer has low survival and eventually develops castration resistance, while androgen deprivation therapy has a limited duration of effectiveness. As a result, CRPC remains incurable despite multiple treatment options.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What role does ferroptosis play in castration-resistant prostate cancer treatment?",{"text":68,"@type":64},"Ferroptosis triggers iron-dependent lipid peroxidation and programmed cell death, and it is discussed as a potential therapeutic target for CRPC. The review also connects ferroptosis mechanisms to treatment responses and prognosis.",{"name":70,"@type":61,"acceptedAnswer":71},"How can ferroptosis influence radiotherapy outcomes in CRPC?",{"text":72,"@type":64},"Ferroptosis is described as crucial for radiation-induced anticancer effects through lipid peroxidation and regulation of pathways involving p53 and AMPK. Inhibiting GPX4 and SLC7A11 is noted to increase radiosensitivity, supporting combination therapy strategies.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},337333,1790852870,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,110,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":107,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":108,"slug":109},7,40,"healthcare",{"id":55,"doc_module":4,"doc_module_name":25,"category_name":111,"show_sort_weight":112,"slug":113},"Research & Report",30,"research-report",{"id":115,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},9,"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},19,"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":107,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":139,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":145},7971461741311,"https://ap-avatar.wpscdn.com/avatar/74000253aff267980c6?x-image-process=image/resize,m_fixed,w_180,h_180&k=1779345379180704826","[www.nature.com/pcan](www.nature.com/pcan Prostate)[ Prostate](www.nature.com/pcan Prostate) Cancer and Prostatic Diseases  \nREVIEW ARTICLE OPEN   \nAdvances in ferroptosis for castration-resistant prostate cancer treatment: novel drug targets and combination therapy strategies  \nHuizhu Chen 1, Feng Lyu1 and Xianshu Gao 1 ✉  \n© The Author(s) 2024  \n\n|  | BACKGROUND: Metastatic prostate cancer (PCa) has much lower survival and ultimately develops castration resistance, which expects novel targets and therapeutic approaches. As a result of iron-dependent lipid peroxidation, ferroptosis triggers programmed cell death and has been associated with castration-resistant prostate cancer (CRPC) .\u003Cbr>SUBJECTS: To better understand how ferroptosis can be used to treat CRPC, we reviewed the following: First, ferroptosis mechanisms and characteristics. We then pay attention to ferroptosis effects on CRPC, and the relationship between ferroptosis and CRPC treatment. Finally, we’d like to ﬁgure out if ferroptosis could predict the prognosis of CRPC thus screening early for populations that may beneﬁt from appropriate therapies.\u003Cbr>RESULTS: The review demonstrated that ferroptosis regulators like PI3K/AKT/mTOR, DECR1 et al., have a signiﬁcant role in the development of CRPC and that several inducers of ferroptosis, such as erastin, BSO, RSL3, and FIN56, have already demonstrated their effects in that area. What’s more, ferroptosis is crucial for radiation-induced anticancer effects by inducing lipid peroxidation and regulating p53, AMPK, and others. Additionally, it has been discovered that certain GPX4 and SLC7A11 inhibitors can increase radiosensitivity, which brings new combination strategies. Finally, among the genes associated with ferroptosis, which may be excellent predictors of prostate cancer prognosis, several risk models have been developed and shown promising predictive capabilities.\u003Cbr>CONCLUSIONS: Ferroptosis can serve as a potential therapeutic target for CRPC, and could be a new strategy for combination therapy Moreover, ferroptosis-related genes may be great indicators of PCa prognosis Further research on ferroptosis in CRPC |  |\n| --- | --- | --- |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n|  |  |  |\n| . .\u003Cbr>therapy can beneﬁt from the frameworks provided by this review. |  |  |\n|  | Prostate Cancer and Prostatic Diseases (2026) 29:36–46; [https://doi.org/10.1038/s41391-024-00933-w](https://doi.org/10.1038/s41391-024-00933-w) |  |\n|  |  |  |\n\nINTRODUCTION  \nThe GLOBOCAN 2020 database reports that among male cancers, PCa ranks second in incidence and ﬁfth in fatalities worldwide [1] . Patients’ chances of surviving PCa are proportional to the stage of the disease when it is ﬁrst diagnosed. According to statistics from the US Surveillance, Epidemiology and End Results Database 2014–2020, patients with clinically localized PCa had a 5-year survival rate of nearly 100% after having standard treatment, which includes radical prostatectomy and radiation. On the other hand, patients with metastatic PCa had a much worse 5-year survival rate of 36%[2]. This is because metastatic PCa eventually develops castration resistance, and androgen deprivation therapy (ADT) has a temporal limit [3] . Until 2004, the only effective medication for improving survival was docetaxel with prednisone. Yet, the enhancement in overall survival remains somewhat restricted [4] . CRPC is still incurable, even though several treatment options have been suggested, such as androgen signaling or synthesis inhibitors (enzalutamide and abiraterone), chemotherapy based on taxanes (docetaxel-DTAX and cabazitaxel), radionuclide therapy that targets the bones (radium-223),  \nand immunotherapy (sipuleucel-T) [5] . Hence, ﬁnding ways to enhance the survival rate of individuals with metastatic PCa is a pressing concern. Consequently, more and more research is","cbCaipeDF5VJU5r6","https://ap.wps.com/l/cbCaipeDF5VJU5r6","pdf",1247553,11,"English","# Background\n# Subjects and Review Focus\n# Results and Key Findings\n## Ferroptosis regulators and inducers in CRPC\n## Ferroptosis in radiation-induced anticancer effects\n## Radiosensitization via GPX4 and SLC7A11 inhibition\n## Ferroptosis-related gene risk models and prognosis\n# Conclusions\n# Introduction\n## Epidemiology and survival of prostate cancer\n## Progression to castration resistance and current therapies\n## Programmed cell death and ferroptosis fundamentals","[{\"question\":\"Why is castration-resistant prostate cancer a major clinical challenge?\",\"answer\":\"Metastatic prostate cancer has low survival and eventually develops castration resistance, while androgen deprivation therapy has a limited duration of effectiveness. As a result, CRPC remains incurable despite multiple treatment options.\"},{\"question\":\"What role does ferroptosis play in castration-resistant prostate cancer treatment?\",\"answer\":\"Ferroptosis triggers iron-dependent lipid peroxidation and programmed cell death, and it is discussed as a potential therapeutic target for CRPC. The review also connects ferroptosis mechanisms to treatment responses and prognosis.\"},{\"question\":\"How can ferroptosis influence radiotherapy outcomes in CRPC?\",\"answer\":\"Ferroptosis is described as crucial for radiation-induced anticancer effects through lipid peroxidation and regulation of pathways involving p53 and AMPK. Inhibiting GPX4 and SLC7A11 is noted to increase radiosensitivity, supporting combination therapy strategies.\"}]","Advances in ferroptosis for castration-resistant prostate cancer treatment: novel drug targets and combination therapy strategies | PDF",1790018623,28]