Inhibitory Aryl Hydrocarbon Receptor−Estrogen Receptor α Cross-Talk and Mechanisms of Action

2003 ◽  
Vol 16 (7) ◽  
pp. 807-816 ◽  
Author(s):  
Stephen Safe ◽  
Mark Wormke
Keyword(s):  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Cross Talk ◽  
Estrogen Receptor Α ◽  
Mechanisms Of Action ◽  
Aryl Hydrocarbon

scholarly journals Estrogen receptor-α and aryl hydrocarbon receptor involvement in the actions of botanical estrogens in target cells

2016 ◽  
Vol 437 ◽  
pp. 190-200 ◽  
Author(s):  
Ping Gong ◽  
Zeynep Madak-Erdogan ◽  
Jodi A. Flaws ◽  
David J. Shapiro ◽  
John A. Katzenellenbogen ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Estrogen Receptor Α ◽  
Target Cells ◽  
Aryl Hydrocarbon

scholarly journals Cross-Talk in the Female Rat Mammary Gland: Influence of Aryl Hydrocarbon Receptor on Estrogen Receptor Signaling

2016 ◽  
Vol 124 (5) ◽  
pp. 601-610 ◽  
Author(s):  
Janina Helle ◽  
Manuela I. Bader ◽  
Annekathrin M. Keiler ◽  
Oliver Zierau ◽  
Günter Vollmer ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Aryl Hydrocarbon Receptor ◽  
Cross Talk ◽  
Female Rat ◽  
Receptor Signaling ◽  
Aryl Hydrocarbon ◽  
Estrogen Receptor Signaling ◽  
Rat Mammary Gland

scholarly journals Aryl Hydrocarbon Receptor-Mediated Transcription: Ligand-Dependent Recruitment of Estrogen Receptor α to 2,3,7,8-Tetrachlorodibenzo- p-Dioxin-Responsive Promoters

2005 ◽  
Vol 25 (13) ◽  
pp. 5317-5328 ◽  
Author(s):  
Jason Matthews ◽  
Björn Wihlén ◽  
Jane Thomsen ◽  
Jan-Åke Gustafsson
Keyword(s):  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Rna Polymerase Ii ◽  
Transcriptional Activation ◽  
Time Course ◽  
Estrogen Receptor Α ◽  
Time Dependent ◽  
Promoter Regions ◽  
Aryl Hydrocarbon ◽  
H3 Acetylation

ABSTRACT Using chromatin immunoprecipitation assays, we studied the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated recruitment of the aryl hydrocarbon receptor (AhR) and several coregulators to the CYP1A1 promoter. AhR displayed a time-dependent recruitment, reaching a peak at 75 min and maintaining promoter occupancy for the remainder of the time course. Recruitment of AhR was followed by TIF2/SRC2, which preceded CBP, histone H3 acetylation, and RNA polymerase II (RNAPII). Simultaneous recruitment to the enhancer and the TATA box region suggests the formation of a large multiprotein complex bridging the two promoter regions. Interestingly, estrogen receptor α (ERα) displayed a TCDD- and time-dependent recruitment to the CYP1A1 promoter, which was increased by cotreatment with estradiol. Transfection in HuH7 human liver cells confirmed previously reported ERα enhancement of AhR activity. In contrast, TCDD did not induce the recruitment of ERα to the estrogen-responsive pS2 promoter, and after 120 min of cotreatment with estradiol, ERα is still present on the CYP1A1 promoter but no longer at pS2. RNA interference studies with T47D cells support a role for ERα in TCDD-dependent CYP1A1 expression. Our data suggest that ERα acts as a coregulator of AhR-mediated transcriptional activation and that the recruitment of ERα by AhR represents a novel mechanism AhR-ERα cross talk.

scholarly journals 3-Methylcholanthrene and Other Aryl Hydrocarbon Receptor Agonists Directly Activate Estrogen Receptor α

2006 ◽  
Vol 66 (4) ◽  
pp. 2459-2467 ◽  
Author(s):  
Maen Abdelrahim ◽  
Eric Ariazi ◽  
Kyounghyun Kim ◽  
Shaheen Khan ◽  
Rola Barhoumi ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Estrogen Receptor Α ◽  
Receptor Agonists ◽  
Aryl Hydrocarbon

scholarly journals The Aryl Hydrocarbon Receptor Mediates Degradation of Estrogen Receptor α through Activation of Proteasomes

2003 ◽  
Vol 23 (6) ◽  
pp. 1843-1855 ◽  
Author(s):  
Mark Wormke ◽  
Matthew Stoner ◽  
Bradley Saville ◽  
Kelcey Walker ◽  
Maen Abdelrahim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Aryl Hydrocarbon

ABSTRACT 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and other aryl hydrocarbon receptor (AhR) ligands suppress 17β-estradiol (E)-induced responses in the rodent uterus and mammary tumors and in human breast cancer cells. Treatment of ZR-75, T47D, and MCF-7 human breast cancer cells with TCDD induces proteasome-dependent degradation of endogenous estrogen receptor α (ERα). The proteasome inhibitors MG132, PSI, and PSII inhibit the proteasome-dependent effects induced by TCDD, whereas the protease inhibitors EST, calpain inhibitor II, and chloroquine do not affect this response. ERα levels in the mouse uterus and breast cancer cells were significantly lower after cotreatment with E plus TCDD than after treatment with E or TCDD alone, and our results indicate that AhR-mediated inhibition of E-induced transactivation is mainly due to limiting levels of ERα in cells cotreated with E plus TCDD. TCDD alone or in combination with E increases formation of ubiquitinated forms of ERα, and both coimmunoprecipitation and mammalian two-hybrid assays demonstrate that TCDD induces interaction of the AhR with ERα in the presence or absence of E. In contrast, E does not induce AhR-ERα interactions. Thus, inhibitory AhR-ERα cross talk is linked to a novel pathway for degradation of ERα in which TCDD initially induces formation of a nuclear AhR complex which coordinately recruits ERα and the proteasome complex, resulting in degradation of both receptors.

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