YAP1 and AR interactions contribute to the switch from androgen-dependent to castration-resistant growth in prostate cancer

Gamze Kuser-Abali, Ahmet Alptekin, Michael Lewis, Isla P. Garraway and Bekir Cinar ()
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Gamze Kuser-Abali: Cancer Biology and Uro-Oncology Programs, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center
Ahmet Alptekin: Cancer Biology and Uro-Oncology Programs, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center
Michael Lewis: West Los Angeles Veteran Affairs Healthcare System
Isla P. Garraway: West Los Angeles Veteran Affairs Healthcare System
Bekir Cinar: Cancer Biology and Uro-Oncology Programs, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract The transcriptional co-activator Yes-associated protein 1 (YAP1), a key nuclear effector of the Hippo pathway, is a potent oncogene, and yet, the interaction between YAP1 and androgen receptor (AR) remains unexplored. Here we identify YAP1 as a physiological binding partner and positive regulator of AR in prostate cancer. YAP1 and AR co-localize and interact with each other predominantly within cell nuclei by an androgen-dependent mechanism in a hormone naive and an androgen-independent mechanism in castration-resistant prostate cancer cells. The growth suppressor MST1 kinase modulates androgen-dependent and -independent nuclear YAP1–AR interactions through directly regulating YAP1 nuclear accumulation. Disruption of YAP1 signalling by genetic (RNAi) and pharmacological (Verteporfin) approaches suppresses AR-dependent gene expression and prostate cancer cell growth. These findings indicate that the YAP1–AR axis may have a critical role in prostate cancer progression and serves as a viable drug target.

Date: 2015
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DOI: 10.1038/ncomms9126

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