Expression of estrogen receptor beta in prostate carcinoma cells inhibits invasion and proliferation and triggers apoptosis

FEBS Lett. 2004 May 21;566(1-3):169-72. doi: 10.1016/j.febslet.2004.04.025.


The involvement of estrogen receptor beta (ERbeta) in prostate carcinogenesis has been hypothesized. Several reports have shown that ERbeta expression was decreased when prostate cells undergo neoplastic transformation, suggesting that it could play a tumor-suppressor role. By restoring ERbeta expression in prostatic carcinoma cells by adenoviral delivery, we aimed to test this hypothesis. We observed that ERbeta strongly inhibited the invasiveness and the growth of these cells. In addition, ERbeta cells were undergoing apoptosis, as shown by quantification of Bax, poly(ADP-ribose) polymerase and caspase-3 expression. Our data suggest that ERbeta acts as a tumor-suppressor by its anti-proliferative, anti-invasive and pro-apoptotic properties.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / genetics
  • Apoptosis / physiology
  • Cell Division / physiology
  • Cell Line, Tumor
  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Gene Expression
  • Humans
  • Immunoblotting
  • Male
  • Neoplasm Invasiveness
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • Receptors, Estrogen / biosynthesis*
  • Receptors, Estrogen / genetics
  • Receptors, Estrogen / metabolism
  • Recombinant Proteins / genetics
  • Recombinant Proteins / metabolism
  • Transfection


  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Receptors, Estrogen
  • Recombinant Proteins