E-cadherin, beta-catenin, and ZEB1 in malignant progression of cancer

Cancer Metastasis Rev. 2009 Jun;28(1-2):151-66. doi: 10.1007/s10555-008-9179-y.

Abstract

The embryonic program 'epithelial-mesenchymal transition' (EMT) is activated during tumor invasion in disseminating cancer cells. Characteristic to these cells is a loss of E-cadherin expression, which can be mediated by EMT-inducing transcriptional repressors, e.g. ZEB1. Consequences of a loss of E-cadherin are an impairment of cell-cell adhesion, which allows detachment of cells, and nuclear localization of beta-catenin. In addition to an accumulation of cancer stem cells, nuclear beta-catenin induces a gene expression pattern favoring tumor invasion, and mounting evidence indicates multiple reciprocal interactions of E-cadherin and beta-catenin with EMT-inducing transcriptional repressors to stabilize an invasive mesenchymal phenotype of epithelial tumor cells.

Publication types

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

MeSH terms

  • Animals
  • Cadherins / metabolism*
  • Cell Adhesion
  • Disease Progression
  • Epithelium / metabolism
  • Gene Expression Regulation, Neoplastic*
  • Homeodomain Proteins / metabolism*
  • Humans
  • Mesoderm / metabolism
  • Models, Biological
  • Neoplasm Invasiveness
  • Neoplasm Metastasis
  • Neoplasms / metabolism*
  • Neoplasms / pathology*
  • Transcription Factors / metabolism*
  • Transcription, Genetic
  • Zinc Finger E-box-Binding Homeobox 1
  • beta Catenin / metabolism*

Substances

  • Cadherins
  • Homeodomain Proteins
  • Transcription Factors
  • ZEB1 protein, human
  • Zinc Finger E-box-Binding Homeobox 1
  • beta Catenin