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Abstract Title:

Estrogen receptor expression is required for low-dose resveratrol-mediated repression of aryl hydrocarbon receptor activity.

Abstract Source:

J Pharmacol Exp Ther. 2010 Nov;335(2):273-83. Epub 2010 Aug 17. PMID: 20716622

Abstract Author(s):

Gary H Perdew, Brett D Hollingshead, Brett C Dinatale, J Luis Morales, Mark P Labrecque, Mandeep K Takhar, Kevin J Tam, Timothy V Beischlag

Article Affiliation:

Faculty of Health Sciences, Blusson Hall, Rm 11311, Simon Fraser University, 8888 University Drive, Burnaby, BC, Canada, V3H 4S3.

Abstract:

The putative cardioprotective and chemopreventive properties of the red wine phenolic resveratrol (RES) have made it the subject of a growing body of clinical and basic research. We have begun investigations focusing on the effects of RES on the activity of the aryl hydrocarbon receptor (AHR) complex. Our evidence suggests that RES is a potent repressor of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible gene transcription in estrogen receptor (ER)-positive human breast, lung, and colon cancer cell lines. RES activates the transcription of the ER target genes to the same degree as estradiol (E(2)) in human MCF-7 breast cancer cells. Unlike E(2), which can only diminish TCDD-inducible CYP1A1 gene transcription by approximately 50%, RES can completely abrogate this response. Furthermore, 50% repression of TCDD-inducible transcription can be achieved with 100 nM RES, approximately 2.5 orders of magnitude lower than concentrations required for maximal inhibition, suggesting that multiple mechanisms are responsible for this effect. RES (100 nM) does not prevent ligand binding of a TCDD analog, nor does it prevent AHR from binding to its response element in the 5'-regulatory region of the CYP1A1 gene. Small inhibitory RNAs directed to ERα have demonstrated that RES-mediated repression of CYP1A1 depends on ERα. Whereas CYP1A1 protein levels in MCF-7 cells are refractory to the low-dose transcriptional effects of RES, a concomitant decrease in CYP1A1 protein levels is observed in Caco-2 cells. These results highlight a low-dose RESeffect that could occur at nutritionally relevant exposures and are distinct from the high-dose effects often characterized.

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Sayer Ji
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