TY - JOUR
T1 - The Ah receptor inhibits estrogen-induced estrogen receptor β in breast cancer cells
AU - Kietz, Silke
AU - Thomsen, Jane S.
AU - Matthews, Jason
AU - Pettersson, Katarina
AU - Ström, Anders
AU - Gustafsson, Jan Åke
N1 - Funding Information:
This research was supported by grants from the Swedish Cancer Fund and from KaroBio AB. S.K. holds an EC Marie Curie individual postdoctoral fellowship (MCFI-2000-02111).
PY - 2004/7/16
Y1 - 2004/7/16
N2 - We have studied the effect of the aryl hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on estrogen receptor (ER) β gene expression in the human breast cancer cell line, T47D. TCDD inhibited 17β-estradiol (E2)-induced up-regulation of both ER β wild type and ER β cx mRNA. Cycloheximide pre-treatment had no inhibitory effect, and the estimated half-life of ER β mRNA of about 33min was not changed by any hormone administration. Chromatin immunoprecipitation experiments showed recruitment of ER α to the ER β promoter. Gel mobility shift experiments revealed an E2-induced protein binding to a half site estrogen response element in the ER β promoter, and TCDD reduced that binding. These results show that ER α regulates the expression of its own heterodimerization partner, ER β, in T47D cells. TCDD, an anti-estrogenic compound, inhibits ER α-mediated induction of ER β mRNA. These findings add to our understanding of cross talk between dioxin and estrogen signaling in human cells.
AB - We have studied the effect of the aryl hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on estrogen receptor (ER) β gene expression in the human breast cancer cell line, T47D. TCDD inhibited 17β-estradiol (E2)-induced up-regulation of both ER β wild type and ER β cx mRNA. Cycloheximide pre-treatment had no inhibitory effect, and the estimated half-life of ER β mRNA of about 33min was not changed by any hormone administration. Chromatin immunoprecipitation experiments showed recruitment of ER α to the ER β promoter. Gel mobility shift experiments revealed an E2-induced protein binding to a half site estrogen response element in the ER β promoter, and TCDD reduced that binding. These results show that ER α regulates the expression of its own heterodimerization partner, ER β, in T47D cells. TCDD, an anti-estrogenic compound, inhibits ER α-mediated induction of ER β mRNA. These findings add to our understanding of cross talk between dioxin and estrogen signaling in human cells.
KW - Aryl hydrocarbon receptor
KW - Breast cancer
KW - Estrogen receptor
KW - Gene expression
KW - Human
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U2 - 10.1016/j.bbrc.2004.05.132
DO - 10.1016/j.bbrc.2004.05.132
M3 - Article
C2 - 15207704
AN - SCOPUS:2942755682
SN - 0006-291X
VL - 320
SP - 76
EP - 82
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -