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Met-HGF/SF mediates growth arrest and differentiation in T47D breast cancer cells

  1. Author:
    Ronen, D.
    Altstock, R. T.
    Firon, M.
    Mittelman, L.
    Sobe, T.
    Resau, J. H.
    Woude, G. F. V.
    Tsarfaty, I.

  2. Author Address

    Tsarfaty I Tel Aviv Univ, Sackler Sch Med, Dept Human Microbiol IL-69978 Ramat Aviv Israel Tel Aviv Univ, Sackler Sch Med, Dept Human Microbiol IL-69978 Ramat Aviv Israel Tel Aviv Univ, Sackler Sch Med, Interdepartmental Core Facil IL-69978 Tel Aviv Israel NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program Frederick, MD 21702 USA
    1. Year: 1999
  2. Journal: Cell Growth and Differentiation
    1. 10
    2. 2
    3. Pages: 131-140
  4. Type of Article: Article
  1. Abstract:

    Hepatocyte growth factor/scatter factor (HGF/SF) is a pluripotent growth factor that exerts mitogenic, motogenic, and morphogenic effects. To elucidate the cellular mechanisms underlying the pluripotent function of this growth factor, T47D human breast cancer cells were transfected with human hgf/sf. The hgf/sf-positive clones exhibited different levels of biologically functional HGF/SF expression and up-regulation of endogenous Met (HGF/SF receptor) expression. In addition, a constitutive phosphorylation of the receptor on tyrosine residues was detected, establishing a Met-HGF/SF autocrine loop. The autocrine activation of Met caused marked inhibition in cell growth accompanied by cell accumulation at G(0)/G(1). These cells underwent terminal cell differentiation as determined by morphological changes, synthesis of milk proteins such as beta-casein and alpha-lactalbumin, and production of lipid vesicles. Our results demonstrate that Met-HGF/SF, an oncogenic signal transduction pathway, is capable of inducing growth arrest and differentiation in certain breast cancer cells and, thus, may have potential as therapeutic and/or prognostic tools in breast cancer treatment. [References: 70]

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