Dietary estrogens act through estrogen receptor-mediated processes and show no antiestrogenicity in cultured breast cancer cells

Dietary estrogens act through estrogen receptor-mediated processes and show no antiestrogenicity in cultured breast cancer cells

Dietary estrogens are believed to exert their estrogenic or antiestrogenic (chemopreventive) action in estrogen responsive cells by interacting with the estrogen receptor (ER). The present study was undertaken to evaluate a direct role of ER in estrogenic or antiestrogenic activities of three dietar...

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Bibliographic Details
Published in:Environmental health perspectives Vol. 102; no. 6/7; pp. 572 - 578
Main Authors: Makela, S, Davis, V.L, Tally, W.C, Korkman, J, Salo, L, Vihko, R, Santti, R, Korach, K.S
Format: Journal Article
Language:English
Published: United States National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare 01-06-1994
Subjects:
Agonists
antiestrogenic properties
Breast cancer
CELL CULTURE
CELL DIVISION
Cell growth
CELL LINES
cell proliferation
CHEMOPROPHYLAXIS
CHIMIOPREVENTION
COUMARINE
COUMARINS
COUMESTROL
CULTIVO DE CELULAS
CULTURE DE CELLULE
Cultured cells
CUMARINAS
DIET
DIETA
DIVISION CELLULAIRE
DIVISION CELULAR
ENFERMEDADES GLANDULAS MAMARIAS
Enzymes
ESTROGENIC PROPERTIES
ESTROGENOS
Estrogens
EXPRESION GENICA
EXPRESSION DES GENES
FLAVONOIDE
FLAVONOIDES
FLAVONOIDS
GENE EXPRESSION
GENISTEIN
HeLa cells
MALADIE DES GLANDES MAMMAIRES
MAMMARY GLAND DISEASES
NEOPLASMAS
NEOPLASME
NEOPLASMS
OESTROGENE
OESTROGENS
Phytoestrogens
PROFILAXIS QUIMICA
ps2 gene
REGIME ALIMENTAIRE
Steroids
T lymphocytes
ZEARALENONA
ZEARALENONE
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Summary:Dietary estrogens are believed to exert their estrogenic or antiestrogenic (chemopreventive) action in estrogen responsive cells by interacting with the estrogen receptor (ER). The present study was undertaken to evaluate a direct role of ER in estrogenic or antiestrogenic activities of three dietary estrogens (coumestrol, genistein and zearalenone). HeLa cells were transiently co-transfected with an expression vector for ER and an estrogen-responsive reporter gene construct. Coumestrol, genistein, and zearalenone all increased the activity of the reporter gene, only in the presence of the ER, and the activation was blocked with the ER antagonist ICI 164,384, demonstrating an ER-specific, agonist response. In addition, in MCF-7 cells, coumestrol and zearalenone increased the expression of the estrogen-responsive pS2 gene. Coumestrol and genistein inhibited the purified estrogen-specific 17β-hydroxysteroid oxidoreductase enzyme and the conversion of estrone to 17β-estradiol in T-47D cells, which contain this enzyme. However, they did not inhibit the estrone-induced proliferation of T-47D cells. In conclusion, coumestrol, genistein, and zearalenone are all potent estrogens in vitro, and they act through ER mediated mechanism. Our findings give no evidence to support the idea that these compounds act as antiestrogens through competition for the binding sites of ER or by inhibition of the conversion of estrone to 17β-estradiol in breast cancer cells, since this effect was nullified by their agonist action on cell proliferation. Therefore, their suggested chemopreventive action in estrogen-related cancers must be mediated through other mechanisms.
Bibliography:S30
9503062
T10
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0091-6765
1552-9924
DOI:10.1289/ehp.94102572