A mechanism for androgen receptor-mediated prostate cancer recurrence after androgen deprivation therapy

Cancer Res. 2001 Jun 1;61(11):4315-9.

Abstract

The development and growth of prostate cancer depends on the androgen receptor and its high-affinity binding of dihydrotestosterone, which derives from testosterone. Most prostate tumors regress after therapy to prevent testosterone production by the testes, but the tumors eventually recur and cause death. A critical question is whether the androgen receptor mediates recurrent tumor growth after androgen deprivation therapy. Here we report that a majority of recurrent prostate cancers express high levels of the androgen receptor and two nuclear receptor coactivators, transcriptional intermediary factor 2 and steroid receptor coactivator 1. Overexpression of these coactivators increases androgen receptor transactivation at physiological concentrations of adrenal androgen. Furthermore, we provide a molecular basis for this activation and suggest a general mechanism for recurrent prostate cancer growth.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aged
  • Androgen Antagonists / therapeutic use
  • Animals
  • Dihydrotestosterone / pharmacology
  • Histone Acetyltransferases
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • Middle Aged
  • Neoplasm Recurrence, Local / metabolism*
  • Neoplasm Recurrence, Local / pathology
  • Neoplasms, Hormone-Dependent / metabolism*
  • Neoplasms, Hormone-Dependent / pathology
  • Neoplasms, Hormone-Dependent / therapy
  • Nuclear Receptor Coactivator 1
  • Nuclear Receptor Coactivator 2
  • Orchiectomy
  • Prostatic Hyperplasia / metabolism
  • Prostatic Hyperplasia / pathology
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • Prostatic Neoplasms / therapy
  • Receptors, Androgen / biosynthesis
  • Receptors, Androgen / physiology*
  • Testosterone / pharmacology
  • Transcription Factors / biosynthesis
  • Transcription Factors / genetics
  • Transcriptional Activation
  • Transplantation, Heterologous

Substances

  • Androgen Antagonists
  • Nuclear Receptor Coactivator 2
  • Receptors, Androgen
  • Transcription Factors
  • Dihydrotestosterone
  • Testosterone
  • Histone Acetyltransferases
  • NCOA1 protein, human
  • Ncoa1 protein, mouse
  • Nuclear Receptor Coactivator 1