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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
Author(s) -
Sasaki Gordon H.,
Leung Benjamin S.
Publication year - 1975
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(197503)35:3<645::aid-cncr2820350316>3.0.co;2-t
Subject(s) - prolactin , medicine , endocrinology , 7,12 dimethylbenz[a]anthracene , estrogen , progesterone receptor , prolactin cell , sephadex , hormone , dmba , in vivo , stimulation , mammary tumor , estrogen receptor , chemistry , biology , biochemistry , breast cancer , carcinogenesis , microbiology and biotechnology , cancer , enzyme
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 present 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.