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

Jennifer Cheng, Eun Jig Lee, Laird D. Madison, Gwendal Lazennec

Research output: Contribution to journalArticle

156 Citations (Scopus)

Abstract

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

Original languageEnglish
Pages (from-to)169-172
Number of pages4
JournalFEBS Letters
Volume566
Issue number1-3
DOIs
Publication statusPublished - 2004 May 21

Fingerprint

Estrogen Receptor beta
Estrogen Receptors
Prostate
Cells
Apoptosis
Carcinoma
Tumors
Neoplastic Cell Transformation
Poly(ADP-ribose) Polymerases
Caspase 3
Neoplasms
Carcinogenesis
Growth

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Cheng, Jennifer ; Lee, Eun Jig ; Madison, Laird D. ; Lazennec, Gwendal. / Expression of estrogen receptor β in prostate carcinoma cells inhibits invasion and proliferation and triggers apoptosis. In: FEBS Letters. 2004 ; Vol. 566, No. 1-3. pp. 169-172.
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Expression of estrogen receptor β in prostate carcinoma cells inhibits invasion and proliferation and triggers apoptosis. / Cheng, Jennifer; Lee, Eun Jig; Madison, Laird D.; Lazennec, Gwendal.

In: FEBS Letters, Vol. 566, No. 1-3, 21.05.2004, p. 169-172.

Research output: Contribution to journalArticle

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