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Diverse Tumorigenesis Associated With Aberrant Development in Mice Overexpressing Hepatocyte Growth Factor Scatter Factor

  1. Author:
    Takayama, H.
    Larochelle, W. J.
    Sharp, R.
    Otsuka, T.
    Kriebel, P.
    Anver, M.
    Aaronson, S. A.
    Merlino, G.

  2. Author Address

    Merlino G NCI MOL GENET SECT MOL BIOL LAB NIH BLDG 37 ROOM 2E24 37 CONVENT DR BETHESDA, MD 20892 USA NCI MOL GENET SECT MOL BIOL LAB NIH BETHESDA, MD 20892 USA NCI CELLULAR & MOL BIOL LAB BETHESDA, MD 20892 USA NCI FREDERICK CANC RES & DEV CTR PATHOL HISTOTECHNOL LAB SCI APPLICAT INT CORP FREDERICK, MD 21702 USA MT SINAI MED CTR RUTTENBERG CANC CTR NEW YORK, NY 10029 USA
    1. Year: 1997
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 94
    2. 2
    3. Pages: 701-706
  4. Type of Article: Article
  1. Abstract:

    Hepatocyte growth factor/scatter factor (HGF/SF) is a mesenchymally derived, multifunctional paracrine regulator possessing mitogenic, mitogenic, and morphogenetic activities in cultured epithelial cells containing its tyrosine kinase receptor, Met, c-met has been implicated in oncogenesis through correlation of expression with malignant phenotype in specific cell lines and tumors, Paradoxically, however, HGF/SF can also inhibit the growth of some tumor cells. To elucidate the oncogenic role of HGF/SF in vivo, transgenic mice were created such that HGF/SF was inappropriately targeted to a variety of tissues, HGF/SF transb genic mice developed a remarkably broad array of histologically distinct tumors of both mesenchymal and epithelial origin, Many neoplasms arose from tissues exhibiting abnormal development, including the mammary gland, skeletal muscle, and melanocytes, suggesting a functional link between mechanisms regulating morphogenesis and those promoting tumorigenesis, Most neoplasms, especially melanomas, demonstrated overexpression of both the HGF/SF transgene and endogenous c-met, and had enhanced Met kinase activity, strongly suggesting that autocrine signaling broadly promotes tumorigenesis. Thus, subversion of normal mesenchymal-epithelial paracrine regulation through the forced misdirection of HGF/SF expression induces aberrant morphogenesis and subsequent malignant transformation of cells of diverse origin. [References: 52]

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