biostudies-literatureObinata DDepartment of Health and Human Services acting through the Victorian Cancer AgencyP-CREATENational Health and Medical Research CouncilNational Health and Medical Research Council, Australiathe Department of Health and Human Services acting through the Victorian Cancer AgencyJapan Society for the Promotion of Science554https://www.ebi.ac.uk/biostudies/studies/S-EPMC11067191biostudies-literatureUnknown24(1)<h4>Background</h4>Prostate cancer is dependent on androgen receptor (AR) signaling, and androgen deprivation therapy (ADT) has proven effective in targeting prostate cancer. However, castration-resistant prostate cancer (CRPC) eventually emerges. AR signaling inhibitors (ARSI) have been also used, but resistance to these agents develops due to genetic AR alterations and epigenetic dysregulation.<h4>Methods</h4>In this study, we investigated the role of OCT1, a member of the OCT family, in an AR-positive CRPC patient-derived xenograft established from a patient with resistance to ARSI and chemotherapy. We conducted a genome-wide analysis chromatin immunoprecipitation followed by sequencing and bioinformatic analyses using public database.<h4>Results</h4>Genome-wide analysis of OCT1 target BMC cancerPatient-derived castration-resistant prostate cancer model revealed CTBP2 upregulation mediated by OCT1 and androgen receptor.PMC11067191MCRF15023JP20K07875JP18ck0106194MCRF18017JP20K21667JP19H037931102752JP19K097401156570Inoue SLawrence MGRisbridger GPTakahashi STaylor RANiranjan BObinata DHara MTakayama KFunakoshi DTeng LfalsePatient-derived castration-resistant prostate cancer model revealed CTBP2 upregulation mediated by OCT1 and androgen receptor.<h4>Background</h4>Prostate cancer is dependent on androgen receptor (AR) signaling, and androgen deprivation therapy (ADT) has proven effective in targeting prostate cancer. However, castration-resistant prostate cancer (CRPC) eventually emerges. AR signaling inhibitors (ARSI) have been also used, but resistance to these agents develops due to genetic AR alterations and epigenetic dysregulation.<h4>Methods</h4>In this study, we investigated the role of OCT1, a member of the OCT family, in an AR-positive CRPC patient-derived xenograft established from a patient with resistance to ARSI and chemotherapy. We conducted a genome-wide analysis chromatin immunoprecipitation followed by sequencing and bioinformatic analyses using public database.<h4>Results</h4>Genome-wide analysis of OCT1 target 2024-01-01T00:00:00Z2024 May2026-07-03T03:23:56.495Z2025-08-28T03:09:02.229ZS-EPMC110671913869834410.1186/s12885-024-12298-3