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  • Title: Estrogenic effects of physiological concentrations of 5-androstene-3 beta, 17 beta-diol and its metabolism in MCF7 human breast cancer cells.
    Author: Adams J, Garcia M, Rochefort H.
    Journal: Cancer Res; 1981 Nov; 41(11 Pt 1):4720-6. PubMed ID: 6458355.
    Abstract:
    5-Androstene-3 beta, 17 beta-diol (ADIOL) has previously been shown to have a high affinity for the estrogen receptor and to translocate it to the nucleus in vitro and in vivo. This compound and related C19 delta 5-steroids of adrenal origin have now been examined for their ability to induce the synthesis in MCF7 cells of an estrogen-dependent secreted glycoprotein (M.W. 46,000). Concentrations required for half-maximum induction were 2 nM for ADIOL and 500 nM for dehydroepiandrosterone (DHEA). Dehydroepiandrosterone sulfate showed weak inducing ability at concentrations of 1 microM or greater. The induction by ADIOL was unaffected by the presence of an aromatase inhibitor, and 5 alpha-androstane-3 beta, 17 beta-diol, which cannot be aromatized, also induced the M.W. 46,000 protein at low concentrations. When cells were exposed to 10 nM [3H]ADIOL, the cytosol and nuclear fractions contained [3H]ADIOL resistant to charcoal adsorption. The bound [3H]ADIOL in the cytosol and nucleus was displaceable by 17 beta-estradiol and tamoxifen, suggesting that it was binding to the estrogen receptor. [3H]ADIOL was metabolized to its 3 beta-sulfate, which was excreted into the medium, and to [3H]DHEA, which was found in the cells and the medium as free DHEA and its 3 beta-sulfate. [3H]DHEA was also metabolized by the cells to its 3 beta-sulfate, to free ADIOL, and to the 3 beta-sulfate of adiol. We conclude that: (a) ADIOL is effective as an estrogen in MCF7 cells at a concentration of 2 nM, which is within the range found in the blood of normal women; and (b) sulfurylation is a major route of inactivation of 3 beta-hydroxy delta 5-steroids in MCF7 cells.
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