The links between axin and carcinogenesis

J Clin Pathol. 2005 Mar;58(3):225-36. doi: 10.1136/jcp.2003.009506.

Abstract

The products of the two mammalian Axin genes (Axin1 and its homologue Axin2) are essential for the degradation of beta catenin, a component of Wnt signalling that is frequently dysregulated in cancer cells. Axin is a multidomain scaffold protein that has many functions in biological signalling pathways. Overexpression of mutant [corrected] axin results in axis duplication in mouse embryos. Wnt signalling activity determines dorsal-ventral axis formation in vertebrates, implicating axin as a negative regulator of this signalling pathway. In addition, Wnts modulate pattern formation and the morphogenesis of most organs by influencing and controlling cell proliferation, motility, and fate. Defects in different components of the Wnt signalling pathway promote tumorigenesis and tumour progression. Recent biochemical studies of axins indicate that these molecules are the primary limiting components of this pathway. This review explores the intriguing connections between defects in axin function and human diseases.

Publication types

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

MeSH terms

  • Animals
  • Axin Protein
  • Cell Transformation, Neoplastic / genetics*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Intercellular Signaling Peptides and Proteins / physiology
  • JNK Mitogen-Activated Protein Kinases / physiology
  • Mice
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / physiology*
  • Repressor Proteins / genetics
  • Repressor Proteins / physiology*
  • Signal Transduction
  • Transforming Growth Factor beta / physiology
  • Wnt Proteins

Substances

  • AXIN1 protein, human
  • Axin Protein
  • Intercellular Signaling Peptides and Proteins
  • Neoplasm Proteins
  • Repressor Proteins
  • Transforming Growth Factor beta
  • Wnt Proteins
  • JNK Mitogen-Activated Protein Kinases