Abstract
The effects of estradiol (E2), dihydrotestosterone (DHT) and dehydro-3-epiandrosterone (DHEA) on proliferation and progesterone receptor induction were studied in a breast cancer cell line (T47D) expressing estrogen, androgen, and progesterone receptors. A significant enhancement of growth and progesterone receptor expression was observed after treatment with E2 and DHEA, which was antagonized by the antiestrogen tamoxifen and not altered by the antiandrogen flutamide, supporting the involvement of estrogen receptors. When cells were treated with either E2 or DHEA, transforming growth factor-alpha mRNA was induced. DHT treatment did not alter growth but was effective in stimulating androgen receptors and down-regulating progesterone receptors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Androgens / pharmacology*
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Breast Neoplasms / chemistry
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Breast Neoplasms / metabolism*
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Breast Neoplasms / pathology*
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Cell Division / drug effects
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Dehydroepiandrosterone / pharmacology
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Dihydrotestosterone / pharmacology
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Down-Regulation
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Estradiol / pharmacology
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Female
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Flutamide / pharmacology
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Humans
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RNA, Messenger / analysis
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Receptors, Androgen / drug effects
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Receptors, Estrogen / drug effects
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Receptors, Estrogen / metabolism*
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Receptors, Progesterone / biosynthesis
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Receptors, Progesterone / drug effects*
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Tamoxifen / pharmacology
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Transforming Growth Factor alpha / biosynthesis
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Tumor Cells, Cultured
Substances
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Androgens
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RNA, Messenger
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Receptors, Androgen
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Receptors, Estrogen
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Receptors, Progesterone
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Transforming Growth Factor alpha
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Dihydrotestosterone
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Tamoxifen
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Dehydroepiandrosterone
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Estradiol
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Flutamide