FEBS Letters | |
Crosstalk between estrogen receptor α and the aryl hydrocarbon receptor in breast cancer cells involves unidirectional activation of proteasomes | |
Safe, Stephen1  Saville, Brad1  Stoner, Matthew1  Wormke, Mark1  | |
[1] Department of Veterinary Physiology and Pharmacology, and Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843-4466, USA | |
关键词: Proteasome; Estrogen receptor α; Aryl hydrocarbon receptor; Degradation; Crosstalk; Breast cancer cell; | |
DOI : 10.1016/S0014-5793(00)01830-5 | |
学科分类:生物化学/生物物理 | |
来源: John Wiley & Sons Ltd. | |
【 摘 要 】
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.
【 授权许可】
Unknown
【 预 览 】
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RO201912020309628ZK.pdf | 291KB | download |