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.

Additional Metadata
Persistent URL dx.doi.org/10.1016/j.ccell.2019.01.008, hdl.handle.net/1765/116113
Journal Cancer Cell
Citation
Cato, L., de Tribolet-Hardy, J., van der Lee, I, Rottenberg, J.T., Coleman, I., Melchers, D, … Brown, M. (2019). ARv7 Represses Tumor-Suppressor Genes in Castration-Resistant Prostate Cancer. Cancer Cell, 35(3), 401–40+. doi:10.1016/j.ccell.2019.01.008