Strategy for Tumor-Selective Disruption of Androgen Receptor Function in the Spectrum of Prostate Cancer
Abstract
Testosterone suppression in prostate cancer is limited by serious side effects and resistance via restoration of androgen receptor (AR) functionality. ELK1 is required for AR-dependent growth in various hormone-dependent and castration-resistant prostate cancer models. The amino-terminal domain of AR docks at two sites on ELK1 to coactivate essential growth genes. This study explores the ability of small molecules to disrupt the ELK1–AR interaction in the spectrum of prostate cancer, inhibiting AR activity in a manner that would predict functional tumor selectivity.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Dec 13, 2018
- Source ID
- 10.1158/1078-0432.ccr-18-0982
Entities
People
- Andrew Fribley
- Benjamin L. Kidder
- Besa Xhabija
- Charles Ducker
- Dakshnamurthy Selvakumar
- Hiroki Kakuta
- Janice Saxton
- Li Jing
- Lisa Polin
- Manohar Ratnam
- Martha Larsen
- Peter E Shaw
- Rayna Rosati
- Seongho Kim
- Thomas Mcfall
- Xun Bao
- Yanfang Huang
Organizations
- National Institutes of Health
- Okayama University
- United States Department of Defense
- University of Michigan
- University of Michigan–Flint
- University of Nottingham
- Wayne State University