Crosstalk between estrogen receptor α and the aryl hydrocarbon receptor in breast cancer cells involves unidirectional activation of proteasomes

Mark Wormke, Matthew Stoner, Brad Saville, Stephen Safe

Research output: Contribution to journalArticle

93 Scopus citations

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxin that activates the aryl hydrocarbon receptor (AhR) and disrupts multiple endocrine signaling pathways. T47D human breast cancer cells express a functional estrogen receptor α (ERα) and AhR, and treatment of these cells with 17β-estradiol (E2) or TCDD resulted in a rapid proteasome-dependent decrease in immunoreactive ERα and AhR proteins (>60-80%), respectively. E2 did not affect the AhR, whereas TCDD induced proteasome-dependent degradation of both the AhR and ERα in T47D and MCF-7 human breast cancer cells, and these responses were specifically blocked by proteasome inhibitors. Thus, TCDD-induced degradation of ERα may contribute to the antiestrogenic activity of AhR agonists and this pathway may be involved in AhR-mediated disruption of other endocrine responses.

Original languageEnglish (US)
Pages (from-to)109-112
Number of pages4
JournalFEBS Letters
Volume478
Issue number1-2
DOIs
StatePublished - Jul 28 2000

Keywords

  • Aryl hydrocarbon receptor
  • Breast cancer cell
  • Crosstalk
  • Degradation
  • Estrogen receptor α
  • Proteasome

ASJC Scopus subject areas

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

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