Premium
Crosstalk between estrogen receptor α and the aryl hydrocarbon receptor in breast cancer cells involves unidirectional activation of proteasomes
Author(s) -
Wormke Mark,
Stoner Matthew,
Saville Brad,
Safe Stephen
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01830-5
Subject(s) - aryl hydrocarbon receptor , estrogen receptor , proteasome , chemistry , receptor , medicine , endocrinology , crosstalk , cancer research , breast cancer , microbiology and biotechnology , biology , cancer , biochemistry , transcription factor , physics , optics , gene
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.