The Ah receptor inhibits estrogen-induced estrogen receptor β in breast cancer cells

Silke Kietz, Jane S. Thomsen, Jason Matthews, Katarina Pettersson, Anders Ström, Jan Åke Gustafsson

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

We have studied the effect of the aryl hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on estrogen receptor (ER) β gene expression in the human breast cancer cell line, T47D. TCDD inhibited 17β-estradiol (E2)-induced up-regulation of both ER β wild type and ER β cx mRNA. Cycloheximide pre-treatment had no inhibitory effect, and the estimated half-life of ER β mRNA of about 33min was not changed by any hormone administration. Chromatin immunoprecipitation experiments showed recruitment of ER α to the ER β promoter. Gel mobility shift experiments revealed an E2-induced protein binding to a half site estrogen response element in the ER β promoter, and TCDD reduced that binding. These results show that ER α regulates the expression of its own heterodimerization partner, ER β, in T47D cells. TCDD, an anti-estrogenic compound, inhibits ER α-mediated induction of ER β mRNA. These findings add to our understanding of cross talk between dioxin and estrogen signaling in human cells.

Original languageEnglish (US)
Pages (from-to)76-82
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume320
Issue number1
DOIs
StatePublished - Jul 16 2004

Keywords

  • Aryl hydrocarbon receptor
  • Breast cancer
  • Estrogen receptor
  • Gene expression
  • Human

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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