Oxidative stress reactivates androgen receptor signaling via USP36 to drive castration resistance in prostate cancer.

ABSTRACT: Castration-resistant prostate cancer (CRPC) often emerges within a few years following androgen deprivation therapy, and therapeutic options remain limited. Androgen deprivation induces oxidative stress in prostate cancer (PCa) cells, leading to aberrant activation of androgen receptor (AR) signaling. This study aims to clarify the molecular mechanism underlying oxidative stress-induced AR activation in CRPC. Transcriptional activity of the prostate-specific antigen (PSA) promoter was evaluated using a dual-luciferase reporter assay under various treatments. To identify AR-interacting proteins under oxidative stress, TurboID-mediated proximity biotin labeling coupled with mass spectrometry was employed following H₂O₂ exposure. Protein-protein interactions between AR a

SUBMITTER: Fan C 

PROVIDER: S-EPMC12658036 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature