Castration resistance in human prostate cancer is conferred by a frequently occurring androgen receptor splice variant.

ABSTRACT: Progression of prostate cancer following castration is associated with increased androgen receptor (AR) expression and signaling despite AR blockade. Recent studies suggest that these activities are due to the generation of constitutively active AR splice variants, but the mechanisms by which these splice variants could mediate such effects are not fully understood. Here we have identified what we believe to be a novel human AR splice variant in which exons 5, 6, and 7 are deleted (ARv567es) and demonstrated that this variant can contribute to cancer progression in human prostate cancer xenograft models in mice following castration. We determined that, in human prostate cancer cell lines, ARv567es functioned as a constitutively active receptor, increased expression of full-length AR (ARfl)

SUBMITTER: Sun S 

PROVIDER: S-EPMC2912187 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature