An endogenous inhibitor of [3H]estradiol binding to nuclear type II estrogen binding sites in normal and malignant tissues.
Previous studies from our laboratory have demonstrated that nonneoplastic tissues, such as rat uterus, contain an endogenous inhibitor of [3H]estradiol binding to nuclear type II sites. Since the stimulation of nuclear type II estrogen binding sites in the rat uterus is highly correlated with the stimulation of uterine growth and DNA synthesis, we have suggested that this inhibitor may be an endogenous ligand for the type II site which may antagonize estrogenic response. The present studies demonstrate that normal mouse mammary gland cytosol contains very high levels of this inhibitor activity, whereas cytosol from mouse mammary tumors and human breast cancer contains very low quantities of this inhibitor. These results are consistent with the observations that rapidly proliferating neoplastic tissue contains very high quantities of nuclear type II sites and that this may be directly related to lower levels of this endogenous inhibitor in these tissues.
D000818:Animals; D002369:Castration; D002467:Cell Nucleus / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D004958:Estradiol / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D007700:Kinetics; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism*; D051379:Mice; D051381:Rats; D011959:Receptors, Estradiol; D011960:Receptors, Estrogen / Q000187:drug effects / Q000302:isolation & purification / Q000378:metabolism*; D014599:Uterus / Q000378:metabolism*
D011959:Receptors, Estradiol; D011960:Receptors, Estrogen; D004958:Estradiol