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Cell Growth & Differentiation, Vol 3, Issue 1 63-71, Copyright © 1992 by American Association of Cancer Research
ARTICLES |
T Venesio, D Taverna, NE Hynes, R Deed, D MacAllan, F Ciardiello, EM Valverius, DS Salomon, R Callahan and G Merlo
National Cancer Institute, NIH, Bethesda, Maryland 20892.
We have investigated the effect of basic fibroblast growth factor (bFGF) and the related int-2 gene on the growth, transformation, and differentiation of HC11 mouse mammary epithelial cells. We show that in HC11 cells infected with int-2 retroviral expression vectors, the int-2 protein can function as a bFGF-like growth factor in stimulating: (a) HC11 cell proliferation in monolayer, (b) anchorage-independent growth in soft agar, and (c) soft agar growth of the bFGF-responsive SW13 tumor cell line. These effects are observed irrespective of whether the int-2 protein is expressed in its wild-type form or is linked to a signal peptide. A candidate bFGF receptor, which is the product of the flg gene and which may recognize the int-2 protein, is expressed at high levels in HC11 cells. Following epidermal growth factor or bFGF priming and subsequent treatment with lactogenic hormones, all of the int-2 infected and the parental HC11 cells synthesize similar levels of beta-casein. However, the autocrine expression of int-2 in HC11 cells abrogates their requirement for either exogenous epidermal growth factor or bFGF priming. These data suggest that, in HC11 cells, the growth factor activity of the int-2 gene is indistinguishable from that of bFGF and does not interfere with the mammary cell differentiation program associated with lactogenesis.
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R Chammas, D Taverna, N Cella, C Santos, and N. Hynes Laminin and tenascin assembly and expression regulate HC11 mouse mammary cell differentiation J. Cell Sci., January 4, 1994; 107(4): 1031 - 1040. [Abstract] [PDF] |
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| Cancer Research | Clinical Cancer Research |
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| Molecular Cancer Research | Cell Growth & Differentiation |