{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li C"],"funding":["U.S. Department of Health &amp; Human Services | NIH | National Cancer Institute","University of Kentucky","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["4498-4511"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9986032"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["41(40)"],"pubmed_abstract":["Prostate cancer (PCa) continues to threaten men's health, and treatment targeting the androgen receptor (AR) pathway is the major therapy for PCa patients. Several second-generation androgen receptor inhibitors (SG-ARIs), including enzalutamide (ENZ), apalutamide (APA) and darolutamide (DARO), have been developed to better block the activity of AR. Unavoidably, emergence of resistance to these novel drugs still persists. Herein, we identified glutathione S-transferase Mu 2 (GSTM2) as an important determinant in the acquisition of resistance to SG-ARIs. Elevated GSTM2 was detected in enzalutamide-resistant (ENZ-R) PCa, and overexpression of GSTM2 in naïve enzalutamide-sensitive (ENZ-S) cells effectively transformed them to ENZ-R PCa. Aryl hydrocarbon receptor (AhR), the upstream transcripti"],"journal":["Oncogene"],"pubmed_title":["GSTM2 is a key molecular determinant of resistance to SG-ARIs."],"pmcid":["PMC9986032"],"funding_grant_id":["P30 CA177558","R01 CA264652","P30CA177558","R01 CA256893","R01 CA196634","R01 CA157429","R35 GM138283"],"pubmed_authors":["Liu J","He D","Li C","Wang C","Lanman NA","Rao X","Mao F","Farah E","Li L","Zhao Y","Liu X","Ngule CM","Zhang Z","Zhang Y","Kazemian M","Kong Y"],"additional_accession":[]},"is_claimable":false,"name":"GSTM2 is a key molecular determinant of resistance to SG-ARIs.","description":"Prostate cancer (PCa) continues to threaten men's health, and treatment targeting the androgen receptor (AR) pathway is the major therapy for PCa patients. Several second-generation androgen receptor inhibitors (SG-ARIs), including enzalutamide (ENZ), apalutamide (APA) and darolutamide (DARO), have been developed to better block the activity of AR. Unavoidably, emergence of resistance to these novel drugs still persists. Herein, we identified glutathione S-transferase Mu 2 (GSTM2) as an important determinant in the acquisition of resistance to SG-ARIs. Elevated GSTM2 was detected in enzalutamide-resistant (ENZ-R) PCa, and overexpression of GSTM2 in naïve enzalutamide-sensitive (ENZ-S) cells effectively transformed them to ENZ-R PCa. Aryl hydrocarbon receptor (AhR), the upstream transcripti","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2025-04-04T00:04:05.053Z","creation":"2025-02-19T02:21:52.429Z"},"accession":"S-EPMC9986032","cross_references":{"pubmed":["36038661"],"doi":["10.1038/s41388-022-02444-1"]}}