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This article has a correction

Please see: J Clin Pathol 2005;58:1344

J Clin Pathol 58:225-236 doi:10.1136/jcp.2003.009506
  • Review

The links between axin and carcinogenesis

  1. S Salahshor,
  2. J R Woodgett
  1. Ontario Cancer Institute, Division of Experimental Therapeutics, Toronto, Ontario, Canada, M5G 2M9
  1. Correspondence to:
 Dr S Salahshor
 Ontario Cancer Institute, Division of Experimental Therapeutics, 610 University Ave, M5G 2M9, Toronto, ON, Canada; SalahshoUhnres.Utoronto.Ca
  • Accepted 26 October 2004

Abstract

The products of the two mammalian Axin genes (Axin1 and its homologue Axin2) are essential for the degradation of β 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 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.

Footnotes