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Medical Breast Cancer Section, Medicine Branck, National Cancer Institute, Bethesda, Maryland [N. E. D., D. A. B., E. P. G., M. E. L.]; Laboratoire de Génétique Moléculaire des Eucaryotes du Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale et Institut de Chimie Biologique, Strasbourg, France [P. C.]; and Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, Maryland [N. E. D.]
Two variants of the human estrogen-responsive breast cancer cell line MCF-7, were utilized to study the expression of an estrogen-induced gene, pS2, and an estrogen-induced Mr 52,000 protein. One variant cell line, I13, is growth inhibited after chronic exposure to estrogen. Both the pS2 gene product and the Mr 52,000 protein were produced at maximal levels at a time when I13 growth was inhibited by estrogen. The variant cell line, LY2, selected for its resistance to the growth-inhibitory effects of the antiestrogen, LY117018, grew normally in the presence of this drug, although both pS2 expression and Mr 52,000 protein production were inhibited. These results confirm that the pS2 gene and Mr 52,000 protein are estrogen-regulated elements, but the lack of correlation between their activities and variant cell growth suggests that they are not major autocrine growth-stimulatory agents.
1 To whom requests for reprints should be addressed, at Building 10, Room 12N226, National Cancer Institute, Bethesda, MD 20205.
Received 7/31/85. Revised 12/30/85. Accepted 1/ 2/86.
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