Tumor formation due to abnormalities in the beta-catenin-independent pathway of Wnt signaling

Cancer Sci. 2008 Feb;99(2):202-8. doi: 10.1111/j.1349-7006.2007.00675.x.

Abstract

Wnt signaling is a complex pathway in which beta-catenin is typically viewed as a central mediator in regulating cell proliferation and differentiation. The significance of Wnt signaling in human cancer has been elucidated by the identification of mutations in genes coding for the beta-catenin-dependent pathway components, adenomatous polyposis coli gene product, beta-catenin, and Axin. Within the past 15 years, evidence has been growing of a beta-catenin-independent pathway in Wnt signaling. It is likely that this pathway activates several intracellular signaling systems to regulate cell migration, adhesion, and polarity. The beta-catenin-independent pathway has also been shown to play an important role in tumor biology. In contrast to the beta-catenin-dependent pathway, which is upregulated in many cancers and serves as a tumor promoter, the role of the beta-catenin-independent pathway is still controversial. Here we review recent developments in both the functions and mechanisms of the beta-catenin-independent pathway, with an emphasis on its functional contribution to human tumor progression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • Calcium / metabolism
  • Dishevelled Proteins
  • Humans
  • Models, Biological
  • Neoplasms / metabolism*
  • Phosphoproteins / metabolism
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Signal Transduction*
  • Wnt Proteins / metabolism*
  • beta Catenin / antagonists & inhibitors
  • beta Catenin / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • Dishevelled Proteins
  • Phosphoproteins
  • Wnt Proteins
  • beta Catenin
  • Receptor Protein-Tyrosine Kinases
  • Calcium