Skip NavigationSkip to Content
Return Return to Search Results

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
  2. Journal: Molecular and Cellular Biology
    1. 21
    2. 17
    3. Pages: 5857-5868
  4. 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.

    See More

  1. Keywords:

External Sources

  1. No sources found.

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel