Journal
CANCER CELL
Volume 17, Issue 6, Pages 535-546Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2010.04.027
Keywords
-
Categories
Funding
- Canadian Institutes of Health Science [MOP79308, PPP90150, MOP89902]
- National Cancer Institute of Canada
- U.S. Army Medical Research and Materiel Command Prostate Cancer Research Program [W81XWH-05-0058, W81XWH-07-1-0260]
- FORE PAR Prostate Awareness Research Charity
- Chief Scientist Office [CZB/4/477] Funding Source: researchfish
Ask authors/readers for more resources
Castration-recurrent prostate cancer (CRPC) is suspected to depend on androgen receptor (AR). The AF-1 region in the amino-terminal domain (NTD) of AR contains most, if not all, of the transcriptional activity. Here we identify EPI-001, a small molecule that blocked transactivation of the NTD and was specific for inhibition of AR without attenuating transcriptional activities of related steroid receptors. EPI-001 interacted with the AF-1 region, inhibited protein-protein interactions with AR, and reduced AR interaction with androgen-response elements on target genes. Importantly, EPI-001 blocked androgen-induced proliferation and caused cytoreduction of CRPC in xenografts dependent on AR for growth and survival without causing toxicity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available