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Oncogenic mutants of RON and MET receptor tyrosine kinases cause activation of the beta-catenin pathway

  1. Author:
    Danilkovitch-Miagkova, A.
    Miagkov, A.
    Skeel, A.
    Nakaigawa, N.
    Zbar, B.
    Leonard, E. J.
  2. Author Address

    NCI, Frederick Canc Res & Dev Ctr, Immunobiol Lab, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Immunobiol Lab, Frederick, MD 21702 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Neuromuscular Div, Baltimore, MD 21231 USA. Danilkovitch-Miagkova A NCI, Frederick Canc Res & Dev Ctr, Immunobiol Lab, Frederick, MD 21702 USA.
    1. Year: 2001
  1. Journal: Molecular and Cellular Biology
    1. 21
    2. 17
    3. Pages: 5857-5868
  2. Type of Article: Review
  1. Abstract:

    beta -Catenin is an oncogenic protein involved in regulation of cell-cell adhesion and gene expression. Accumulation of cellular beta -catenin occurs in many types of human cancers. Four mechanisms are known to cause increases in beta -catenin: mutations of beta -catenin, adenomatous polyposis coli, or axin genes and activation of Wnt signaling. We report a new cause of beta -catenin accumulation involving oncogenic mutants of RON and MET receptor tyrosine kinases (RTKs). Cells transfected with oncogenic RON or MET were characterized by beta -catenin tyrosine phosphorylation and accumulation; constitutive activation of a Tcf transcriptional factor; and increased levels of beta -catenin/Tcf target oncogene proteins c-myc and cyclin D1. Interference with the beta -catenin pathway reduced the transforming potential of mutated RON and MET. Activation of beta -catenin by oncogenic RON and MET constitutes a new pathway, which might lead to cell transformation by these and other mutant growth factor RTKs.

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