Regulation of Estrogen Receptors in Ovarian-Dependent Rat Mammary Tumors. I. Effects of Castration and Prolactin

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Abstract
The ovarian-dependent rat mammary tumors, induced by 9,10 dimethyl-1,2-benzanthracene, were assayed for their estrogen receptor content by dextran-coated charcoal adsorption and sucrose gradient ultracentrifugation. The estradiol receptors bound estrogens with a high affinity .simeq. 0.25 nM), limited capacity and high specificity, and sediment at 8 S in a sucrose gradient. The cytosol receptors were transferred to the nucleus after binding to estrogens in vivo or in vitro. The tumor area regressed by 70% during the 1st 10 days of castration while the concentration of estradiol cytosol receptors decreased from 225 to 16 fmol/mg of protein. Three to 5 days after in vivo administration of estradiol (2 .mu.g daily) or prolactin (1 mg daily) the concentration of estrogen receptors was increased in spayed rats. In biopsy experiments, prolactin, but not estradiol, increased the estrogen receptor concentration when endogenous prolactin release was blocked by CB 154 [2-bromo-.alpha.-ergocryptine]. Prolactin did not modify the intracellular distribution of the estrogen receptor or its binding affinity for estrogen. The uterine estrogen receptor sites were not modified by prolactin under the same conditions. In mammary tumors prolactin sensitizes the action of estrogens at the target level by increasing the concentration of their available receptor sites.

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