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Stabilization of beta-catenin by genetic defects in melanoma cell lines.

Author information

Affiliations

  • 1. Onyx Pharmaceuticals, 3031 Research Drive, Richmond, CA 94806, USA.
      Authors
    • Rubinfeld B 1
    (1 author)

Science, 01 Mar 1997, 275(5307):1790-1792
https://doi.org/10.1126/science.275.5307.1790 PMID: 9065403 

A comment on this article appears in "Beta-catenin as oncogene: the smoking gun." Science. 1997 Mar 21;275(5307):1752-3.

Abstract 

Signal transduction by beta-catenin involves its posttranslational stabilization and downstream coupling to the Lef and Tcf transcription factors. Abnormally high amounts of beta-catenin were detected in 7 of 26 human melanoma cell lines. Unusual messenger RNA splicing and missense mutations in the beta-catenin gene (CTNNB1) that result in stabilization of the protein were identified in six of the lines, and the adenomatous polyposis coli tumor suppressor protein (APC) was altered or missing in two others. In the APC-deficient cells, ectopic expression of wild-type APC eliminated the excess beta-catenin. Cells with stabilized beta-catenin contained a constitutive beta-catenin-Lef-1 complex. Thus, genetic defects that result in up-regulation of beta-catenin may play a role in melanoma progression.

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Read article at publisher's site: https://doi.org/10.1126/science.275.5307.1790

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Funding 

Funders who supported this work.

NCI NIH HHS (1)