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 language | English (US) |
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Pages (from-to) | 109-112 |
Number of pages | 4 |
Journal | FEBS Letters |
Volume | 478 |
Issue number | 1-2 |
DOIs | |
State | Published - 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