{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T02:40:00Z","timestamp":1781664000189,"version":"3.54.5"},"reference-count":45,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2024,5,7]],"date-time":"2024-05-07T00:00:00Z","timestamp":1715040000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81402282"],"award-info":[{"award-number":["81402282"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FEBS Journal"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:p>\n                    Docetaxel (Doc) currently serves as the primary first\u2010line treatment for patients with castrate\u2010resistant prostate cancer (CRPC). Erastin, a small molecule compound, can trigger inhibition of the cystine\u2013glutamate reverse transport system and other pathways, leading to iron\u2010dependent cell death (ferroptosis). Beyond its role in inducing cancer cell death, erastin demonstrates potential when combined with chemotherapy drugs to heighten cancer cell drug susceptibility. However, the augmentation by erastin of the effects of Doc treatment on prostate cancer, and the underlying mechanisms involved, remain unclear. In the present study, we determined the role and the underlying molecular mechanism of erastin against CRPC. The results showed that CRPC cell lines were resistant to Doc, and the expression of ferroptosis\u2010related factors in drug\u2010resistant cell lines was downregulated. Erastin, in synergy with Doc, exerts a pro\u2010apoptotic effect. Erastin significantly inhibited the activity of ATP\u2010binding cassette subfamily B member 1 (ABCB1) but did not change its protein expression and localization. Finally, in mice, erastin treatment dramatically reduced tumor growth\n                    <jats:italic>in\u2009vivo<\/jats:italic>\n                    . Taken together, our findings demonstrate that erastin enhances Doc\u2010induced apoptosis to a certain extent and reverses Doc resistance in prostate cancer by inhibiting the activity of multidrug\u2010resistant protein ABCB1.\n                  <\/jats:p>","DOI":"10.1111\/febs.17135","type":"journal-article","created":{"date-parts":[[2024,5,7]],"date-time":"2024-05-07T04:49:40Z","timestamp":1715057380000},"page":"3249-3266","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["<scp>ABCB<\/scp>\n                    1\u2010mediated docetaxel resistance reversed by erastin in prostate cancer"],"prefix":"10.1111","volume":"291","author":[{"given":"Fangfang","family":"Chen","sequence":"first","affiliation":[{"name":"Institution of Life Sciences Chongqing Medical University  China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shiqi","family":"Wu","sequence":"additional","affiliation":[{"name":"Institution 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