Androgen deprivation therapy for prostate cancer (PCa) benefits patients with early disease, but becomes ineffective as PCa progresses to a castration-resistant state (CRPC). Initially CRPC remains dependent on androgen receptor (AR) signaling, often through increased expression of full-length AR (ARfl) or expression of dominantly active splice variants such as ARv7. We show in ARv7-dependent CRPC models that ARv7 binds together with ARfl to repress transcription of a set of growth-suppressive genes. Expression of the ARv7-repressed targets and ARv7 protein expression are negatively correlated and predicts for outcome in PCa patients. Our results provide insights into the role of ARv7 in CRPC and define a set of potential biomarkers for tumors dependent on ARv7. Display omitted •ARfl and ARv7 genomic binding is interdependent and colocalized•ARv7, unlike ARfl, preferentially represses transcription•Expression of ARv7-repressed genes negatively correlates with recurrence•Re-expression of ARv7-repressed genes may serve as a biomarker of ARv7 inhibition Cato et al. utilize cistrome and transcriptome analyses in castration-resistant prostate cancer (CRPC) to reveal that the androgen receptor (AR) splice variant ARv7 functions as a transcriptional repressor and heterodimerizes with full-length AR at a subset of growth-suppressive genes to support CRPC growth.