Document Detail

Estrogen and aryl hydrocarbon receptor expression and crosstalk in human Ishikawa endometrial cancer cells.
MedLine Citation:
PMID:  10822009     Owner:  NLM     Status:  MEDLINE    
Ishikawa endometrial cancer cells express the estrogen receptor (ER), and this study investigates aryl hydrocarbon receptor (AhR) expression and inhibitory AhR-ER crosstalk in this cell line. Treatment of Ishikawa cells with the AhR agonist [3H]2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) gave a radiolabeled nuclear complex that sedimented at 6.0 S in sucrose density gradients, and Western blot analysis confirmed that Ishikawa cells expressed human AhR and AhR nuclear translocator (Arnt) proteins. Treatment of Ishikawa cells with 10 nM TCDD induced a 9.7-fold increase in CYP1A1-dependent ethoxyresorufin O-deethylase (EROD) activity and a 10.5-fold increase in chloramphenicol acetyltransferase (CAT) activity in cells transfected with pRNH11c containing an Ah-responsive human CYP1A1 gene promoter insert (-1142 to +2434). Inhibitory AhR-ER crosstalk was investigated in Ishikawa cells using E2-induced cell proliferation and transcriptional activation assays in cells transfected with E2-responsive constructs containing promoter inserts from the progesterone receptor and vitellogenin A2 genes. AhR agonists including TCDD, benzo[a]pyrene (BaP) and 6-methyl-1,3,8-trichlorodibenzofuran, inhibited 32-47% of the E2-induced responses. In contrast, neither estrogen nor progesterone inhibited EROD activity induced by TCDD in Ishikawa cells, whereas inhibitory ER-AhR crosstalk was observed in ECC-1 endometrial cells suggesting that these interactions were cell context-dependent.
M Wormke; E Castro-Rivera; I Chen; S Safe
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of steroid biochemistry and molecular biology     Volume:  72     ISSN:  0960-0760     ISO Abbreviation:  J. Steroid Biochem. Mol. Biol.     Publication Date:  2000 Apr 
Date Detail:
Created Date:  2000-07-06     Completed Date:  2000-07-06     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9015483     Medline TA:  J Steroid Biochem Mol Biol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  197-207     Citation Subset:  IM    
Department of Veterinary Physiology and Pharmacology, Texas A & M University, TX 77843-4466, College Station, USA.
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MeSH Terms
Adenocarcinoma / drug therapy,  genetics,  metabolism*
Aryl Hydrocarbon Receptor Nuclear Translocator
Benzo(a)pyrene / pharmacology
Benzofurans / pharmacology
Chloramphenicol O-Acetyltransferase / drug effects,  genetics,  metabolism
Cytochrome P-450 CYP1A1 / drug effects,  genetics,  metabolism
DNA-Binding Proteins*
Endometrial Neoplasms / drug therapy,  genetics,  metabolism*
Estradiol / pharmacology
Promoter Regions, Genetic
Receptors, Aryl Hydrocarbon / agonists,  genetics,  metabolism*
Receptors, Estrogen / drug effects,  genetics,  metabolism*
Receptors, Progesterone / drug effects,  genetics,  metabolism
Tetrachlorodibenzodioxin / pharmacology
Transcription Factors / drug effects,  metabolism
Transcription, Genetic
Tumor Cells, Cultured
Grant Support
Reg. No./Substance:
0/ARNT protein, human; 0/Benzofurans; 0/DNA-Binding Proteins; 0/Receptors, Aryl Hydrocarbon; 0/Receptors, Estrogen; 0/Receptors, Progesterone; 0/Transcription Factors; 115039-00-4/6-methyl-1,3,8-trichlorodibenzofuran; 138391-32-9/Aryl Hydrocarbon Receptor Nuclear Translocator; 1746-01-6/Tetrachlorodibenzodioxin; 50-28-2/Estradiol; 50-32-8/Benzo(a)pyrene; EC P-450 CYP1A1; EC O-Acetyltransferase

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