On the mechanism of hormone action in 7,12 dimethylbenz(a)anthracene-induced mammary tumor. I. Prolactin and progesterone effects on estrogen receptor in vitro.
The presence of ER in DMBA-tumors was demonstrated by the use of dextran-charcoal assay, sephadex chromatography, sucrose gradient sedimentation, and organ culture techniques. It was found that tumors have binding sites ranging from 10-13 to 10-15 moles/mg protein, and a dissociation constant of ER 10-9 to 10-10 M. In experiments with tumor explants, prolactin-insulin significantly stimulated ER binding capacity, as compared with control without prolactin. This stimulation was tissue-specific and inhibited by progesterone. Insulin had a synergistic effect on prolactin stimulation of ER. Our results presents a plausible explanation for tumor responses to these hormones in vivo. This interaction of prolactin, estrogen, and progesterone may be a common phenomenon for all estrogen-responsive tissues.
D000818:Animals; D001551:Benz(a)Anthracenes; D002499:Centrifugation, Density Gradient; D002850:Chromatography, Gel; D004357:Drug Synergism; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D007328:Insulin / Q000494:pharmacology; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology*; D011388:Prolactin / Q000494:pharmacology*; D051381:Rats; D011956:Receptors, Cell Surface; D013268:Stimulation, Chemical
D001551:Benz(a)Anthracenes; D007328:Insulin; D011956:Receptors, Cell Surface; D011374:Progesterone; D004958:Estradiol; D011388:Prolactin