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Effect of Prolactin on Growth and the Estrogen Receptor Level of Human Breast Cancer Cells (MCF-7)¹

Department of Biochemistry, Wayne State University School of Medicine [S. S., S. C. B.], and The Michigan Cancer Foundation [S. C. B.], Detroit, Michigan 48201

The intracellular specific 17ß-estradiol binding in the human breast cancer cell line, MCF-7, was shown to be modified by prolactin. Both ovine and human prolactin doubled the estradiol receptor (E₂R) level, but the latter was at least 10 times more stimulatory on a concentration basis. Most of the E₂R complex (approximately 80%) was transported to the nucleus, and the prolactin stimulation was reflected in an elevated nuclear uptake of the tritiated 17ß-estradiol. Neither ovine nor human prolactin altered the growth rate of the cells when E₂R stimulation was maximal. Insulin (10 µg/ml) stimulated tritiated thymidine incorporation and total DNA content but had no apparent effect on E₂R concentration. At 10^–4 M, N⁶,O²'-dibutyrylcyclicadenosine 3':5'-monophosphate increased insulin stimulation of tritiated thymidine incorporation and brought about a prolactin stimulation of apparent DNA synthesis. Theophylline (10^–3 M) blocked both of these effects of N⁶,O²'-dibutyrylcyclicadenosine 3':5'-monophosphate. The possible mechanism implicating prolactin as an effect of differentiation and growth of MCF-7 cells is discussed.

¹ This investigation was supported in part by USPHS Research Grant CA 07177 from the National Cancer Institute.

² Present address: Department of Biochemistry, University of Rochester School of Medicine, Rochester, N. Y. 14642.

Received 8/ 6/76. Accepted 12/13/76.

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