Targeting GRP78-dependent AR-V7 protein degradation overcomes castration-resistance in prostate cancer therapy.

ABSTRACT: Rationale: Androgen receptor splice variant 7 (AR-V7) is a leading cause of the development of castration-resistant prostate cancer (CRPC). However, the regulation and function of AR-V7 at levels of post-translational modifications in prostate cancer therapy remain poorly understood. Here, we conducted a library screen of natural products to identify potential small molecules responsible for AR-V7 protein degradation in human prostate cancer cell lines. Methods: A natural product library was used to screen the inhibitor of AR-V7. Co-IP and biomass spectrum assays were used to identify the AR-V7-interacting proteins, whereas western blot, confocal microscopy, RNA interfering, and gene transfection were used to validate these interactions. Cell viability, EDU staining, and colo

SUBMITTER: Liao Y 

PROVIDER: S-EPMC7069092 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature