{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bai L"],"funding":["National Cancer Institute","National Institute on Minority Health and Health Disparities","U.S. Department of Education"],"pagination":["101707"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10248552"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["34"],"pubmed_abstract":["Chemoresistance is a major obstacle in the clinical management of metastatic, castration-resistant prostate cancer (PCa). It is imperative to develop novel strategies to overcome chemoresistance and improve clinical outcomes in patients who have failed chemotherapy. Using a two-tier phenotypic screening platform, we identified bromocriptine mesylate as a potent and selective inhibitor of chemoresistant PCa cells. Bromocriptine effectively induced cell cycle arrest and activated apoptosis in chemoresistant PCa cells but not in chemoresponsive PCa cells. RNA-seq analyses revealed that bromocriptine affected a subset of genes implicated in the regulation of the cell cycle, DNA repair, and cell death. Interestingly, approximately one-third (50/157) of the differentially expressed genes affecte"],"journal":["Translational oncology"],"pubmed_title":["Bromocriptine monotherapy overcomes prostate cancer chemoresistance in preclinical models."],"pmcid":["PMC10248552"],"funding_grant_id":["5U54MD007590","R01CA256058","R42CA217491"],"pubmed_authors":["White EZ","Hinton CV","Li D","Wu AY","Du Y","Wu D","Li X","Cook N","Yang Y","Zhao R","Fu H","Bai L","Danaher A","Bowen NJ","Kucuk O","Qui M"],"additional_accession":[]},"is_claimable":false,"name":"Bromocriptine monotherapy overcomes prostate cancer chemoresistance in preclinical models.","description":"Chemoresistance is a major obstacle in the clinical management of metastatic, castration-resistant prostate cancer (PCa). It is imperative to develop novel strategies to overcome chemoresistance and improve clinical outcomes in patients who have failed chemotherapy. Using a two-tier phenotypic screening platform, we identified bromocriptine mesylate as a potent and selective inhibitor of chemoresistant PCa cells. Bromocriptine effectively induced cell cycle arrest and activated apoptosis in chemoresistant PCa cells but not in chemoresponsive PCa cells. RNA-seq analyses revealed that bromocriptine affected a subset of genes implicated in the regulation of the cell cycle, DNA repair, and cell death. Interestingly, approximately one-third (50/157) of the differentially expressed genes affecte","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jun","modification":"2025-04-27T02:19:11.165Z","creation":"2025-04-06T18:31:05.09Z"},"accession":"S-EPMC10248552","cross_references":{"pubmed":["37271121"],"doi":["10.1016/j.tranon.2023.101707"]}}