Tumour-stroma interactions in colorectal cancer: converging on beta-catenin activation and cancer stemness

Br J Cancer. 2008 Jun 17;98(12):1886-93. doi: 10.1038/sj.bjc.6604401. Epub 2008 May 27.

Abstract

Sporadic cases of colorectal cancer are primarily initiated by gene mutations in members of the canonical Wnt pathway, ultimately resulting in beta-catenin stabilisation. Nevertheless, cells displaying nuclear beta-catenin accumulation are nonrandomly distributed throughout the tumour mass and preferentially localise along the invasive front where parenchymal cells are in direct contact with the stromal microenvironment. Here, we discuss the putative role played by stromal cell types in regulating beta-catenin intracellular accumulation in a paracrine fashion. As such, the tumour microenvironment is likely to maintain the cancer stem cell phenotype in a subset of cells, thus mediating invasion and metastasis.

Publication types

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

MeSH terms

  • Adipocytes / cytology
  • Colorectal Neoplasms / immunology
  • Colorectal Neoplasms / metabolism
  • Colorectal Neoplasms / pathology*
  • Humans
  • Neoplasm Invasiveness
  • Neoplasm Metastasis
  • Neoplastic Stem Cells / metabolism
  • Neoplastic Stem Cells / pathology*
  • Stromal Cells / metabolism
  • Stromal Cells / pathology*
  • beta Catenin / metabolism*

Substances

  • beta Catenin