Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells

Cancer Lett. 2004 Sep 30;213(2):155-63. doi: 10.1016/j.canlet.2004.04.003.

Abstract

Previously, we reported that quercetin and resveratrol inhibit the function of androgen receptor (AR). Further studies showed that these two polyphenols caused an increase in expression of c-Jun as well as its phosphorylated form in a dose-dependent manner in prostatic cell lines. Gel shift assay showed that induced c-Jun has specific DNA binding activity. Transient transfections demonstrated that c-Jun repressed prostate-specific antigen promoter activity and transcriptional activity of the AR promoter. These results support a mechanism in which overexpressed c-Jun mediates inhibitory effect on the function of AR. These polyphenols might potentially be useful in prostate cancer prevention.

Publication types

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

MeSH terms

  • Angiogenesis Inhibitors / pharmacology
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Humans
  • Male
  • Phenols
  • Prostatic Neoplasms / pathology*
  • Proto-Oncogene Proteins c-jun / biosynthesis*
  • Quercetin / pharmacology*
  • Receptors, Androgen / drug effects*
  • Receptors, Androgen / physiology*
  • Resveratrol
  • Stilbenes / pharmacology*
  • Transcription, Genetic / drug effects
  • Tumor Cells, Cultured
  • Up-Regulation

Substances

  • Angiogenesis Inhibitors
  • Antineoplastic Agents, Phytogenic
  • Phenols
  • Proto-Oncogene Proteins c-jun
  • Receptors, Androgen
  • Stilbenes
  • Quercetin
  • Resveratrol