Inhibiting androgen receptor nuclear entry in castration-resistant prostate cancer

Julie A. Pollock, Suzanne E. Wardell, Alexander A. Parent, David B. Stagg, Stephanie J. Ellison, Holly M. Alley, Christina A. Chao, Scott A. Lawrence, James P. Stice, Ivan Spasojevic, Jennifer G. Baker, Sung Hoon Kim, Donald P. McDonnell, John A. Katzenellenbogen, John D. Norris

Research output: Contribution to journalArticlepeer-review

Abstract

Clinical resistance to the second-generation antiandrogen enzalutamide in castration-resistant prostate cancer (CRPC), despite persistent androgen receptor (AR) activity in tumors, highlights an unmet medical need for next-generation antagonists. We have identified and characterized tetra-aryl cyclobutanes (CBs) as a new class of competitive AR antagonists that exhibit a unique mechanism of action. These CBs are structurally distinct from current antiandrogens (hydroxyflutamide, bicalutamide, and enzalutamide) and inhibit AR-mediated gene expression, cell proliferation, and tumor growth in several models of CRPC. Conformational profiling revealed that CBs stabilize an AR conformation resembling an unliganded receptor. Using a variety of techniques, it was determined that the AR-CB complex was not recruited to AR-regulated promoters and, like apo AR, remains sequestered in the cytoplasm, bound to heat shock proteins. Thus, we have identified third-generation AR antagonists whose unique mechanism of action suggests that they may have therapeutic potential in CRPC. - 2016 Nature America, Inc.

Original languageEnglish (US)
Pages (from-to)795-801
Number of pages7
JournalNature chemical biology
Volume12
Issue number10
DOIs
StatePublished - Oct 1 2016

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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