{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ota H"],"funding":["Japan Agency for Medical Research and Development"],"pagination":["11618"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10354070"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Androgen deprivation therapy is given to suppress prostate cancer growth; however, some cells continue to grow hormone-independently as castration-resistant prostate cancer (CRPC). Sulfated glycosaminoglycans promote ligand binding to receptors as co-receptors, but their role in CRPC remains unknown. Using the human prostate cancer cell line C4-2, which can proliferate in hormone-dependent and hormone-independent conditions, we found that epidermal growth factor (EGF)-activated EGFR-ERK1/2 signaling via 3-O-sulfated heparan sulfate (HS) produced by HS 3-O-sulfotransferase 1 (HS3ST1) is activated in C4-2 cells under hormone depletion. Knockdown of HS3ST1 in C4-2 cells suppressed hormone-independent growth, and inhibited both EGF binding to the cell surface and activation of EGFR-ERK1/2 sign"],"journal":["Scientific reports"],"pubmed_title":["Switching mechanism from AR to EGFR signaling via 3-O-sulfated heparan sulfate in castration-resistant prostate cancer."],"pmcid":["PMC10354070"],"funding_grant_id":["JP20ae0101037"],"pubmed_authors":["Wakai K","Yamamoto K","Mizumoto S","Yamada S","Ikeda JI","Ota H","Nishihara S","Takahashi S","Nakanishi H","Yoneda K","Ichikawa T","Sato H","Sakamoto S","Ikehara Y"],"additional_accession":[]},"is_claimable":false,"name":"Switching mechanism from AR to EGFR signaling via 3-O-sulfated heparan sulfate in castration-resistant prostate cancer.","description":"Androgen deprivation therapy is given to suppress prostate cancer growth; however, some cells continue to grow hormone-independently as castration-resistant prostate cancer (CRPC). Sulfated glycosaminoglycans promote ligand binding to receptors as co-receptors, but their role in CRPC remains unknown. Using the human prostate cancer cell line C4-2, which can proliferate in hormone-dependent and hormone-independent conditions, we found that epidermal growth factor (EGF)-activated EGFR-ERK1/2 signaling via 3-O-sulfated heparan sulfate (HS) produced by HS 3-O-sulfotransferase 1 (HS3ST1) is activated in C4-2 cells under hormone depletion. Knockdown of HS3ST1 in C4-2 cells suppressed hormone-independent growth, and inhibited both EGF binding to the cell surface and activation of EGFR-ERK1/2 sign","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2025-07-02T03:04:35.097Z","creation":"2025-04-06T18:41:03.876Z"},"accession":"S-EPMC10354070","cross_references":{"pubmed":["37463954"],"doi":["10.1038/s41598-023-38746-x"]}}