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Department of Developmental Biology, Genentech, Inc., South San Francisco, California 94080 [B. A. A., R. D.] Cancer Research Institute, University of California, San Francisco, California 94143 [B. A. A.]; and Departments of Medicine and Biochemistry, University of California, Irvine, California 92717 [M. K.]
Transforming growth factor (TGF)-ß is a potent regulator of many cell functions and a growth inhibitor for mammary epithelial cells. We now know of three highly homologous members of the human TGF-ß gene family. We have studied the expression of TGF-ß1, -ß2, and -ß3 mRNA in four human breast cancer cell lines. Using the RNase protection assay, we have detected mRNA expression of TGF-ß1, -ß2, and -ß3 by T-47D cells, TGF-ß1 and -ß3 by ZR-75-1 cells, and TGF-ß1 by MCF-7 cells. Treatment of these estrogen receptor-positive cells with 10 nM estradiol for 48 h resulted in decreased mRNA levels of TGF-ß2 and -ß3 but did not affect mRNA levels of TGF-ß1. Expression of TGF-ß1 and -ß2 mRNA by an estrogen receptor-negative cell line, MDA-MB-231, was not changed by estradiol treatment. Treatment of cells with the antiestrogen tamoxifen (1 µM) did not significantly alter mRNA levels for any of the three TGF-ß species. We have further determined that estradiol treatment of T-47D was associated with diminished secretion of TGF-ß into the medium. Both TGF-ß1 and -ß2 inhibited the proliferation of MCF-7 cells, and neither protein affected the growth of T-47D cells. TGF-ß1 was at least 10-fold more potent than TGF-ß2 at inhibiting the growth of MCF-7 cells.
1 To whom requests for reprints should be addressed, at Department of Developmental Biology, Genentech, Inc., 460 Point San Bruno Blvd., South San Francisco, CA 94080.
2 Supported by National Cancer Institute Grant CA 40162. On sabbatical leave from the University of Arizona.
Received 5/22/89. Revised 9/13/89. Accepted 10/12/89.
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