期刊
CANCER DISCOVERY
卷 9, 期 11, 页码 1490-1492出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2159-8290.CD-19-1028
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资金
- NIH [P01 CA163227, P50 CA090381]
- Department of Defense Prostate Cancer Research Program [W81XWH-16-1-0431]
- Early Investigator Research Award [PC170570]
- A. David Mazzone Research Awards Program
- Prostate Cancer Foundation
In this issue of Cancer Discovery, Rasool and colleagues show that TF11H/CDK7 phosphorylates the MED1 component of the Mediator complex, which enhances its interaction with androgen receptor (AR), and that this phosphorylation is increased in prostate cancer that is resistant to castration and enzalutamide. A covalent CDK7-specific inhibitor (THZ1) impairs AR-mediated MED1 recruitment to chromatin, and can suppress enzalutamide resistance in vitro and induce tumor regression in a castration-resistant prostate cancer xenograft model, suggesting a novel therapeutic approach for advanced prostate cancer.
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