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Evidence of an EGF/TGF-α—independent pathway for estrogen-regulated cell proliferation

✍ Scribed by B. S. Leung; L. Stout; L. Zhou; H. J. Ji; Q. Q. Zhang; H. T. Leung

Publisher
John Wiley and Sons
Year
1991
Tongue
English
Weight
745 KB
Volume
46
Category
Article
ISSN
0730-2312

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✦ Synopsis

To elucidate the relationship between epidermal growth factor (EGF)/transforming growth factor (TGF-a) and estradiol-17p (E) in cell proliferation, we examined their effects on the breast cancer cell line, CAMA-1. While E was able to consistently induce cell proliferation under a variety of experimental conditions, EGF/TGF-a was without effect. Despite the presence of the receptor (EGFR) gene, mature EGFR protein and mRNA were not detected by radioreceptor assay, 35S Met-labelling, and the lntron Differential RNNPCR method under conditions in which cells remain responsive to E. Furthermore, TGF-a is not an autocrine factor in CAMA-1 cells. We demonstrated unequivocally that EGFDGF-a interaction with EGFR is not an obligatory event in mediating estrogen-stimulated cell proliferation.

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