Molecular mechanisms controlling E-cadherin expression in breast cancer

Biochem Biophys Res Commun. 2009 Jun 19;384(1):6-11. doi: 10.1016/j.bbrc.2009.04.051. Epub 2009 Apr 18.


Disruption of cell-cell adhesion, which is essential for the maintenance of epithelial plasticity and is mediated by a class of proteins called cadherins, is an initial event in the progression of cancer. Cadherins are Ca(2+)-dependent transmembrane proteins that are associated with actin via other cytoplasmic proteins. Disruption of cell-cell adhesion during cancer progression is an important event during cancer initiation and metastasis. E-cadherin, one of the most widely studied tumor suppressors in breast cancer, belongs to a family of calcium-dependent cell adhesion molecules. Various signaling molecules and transcription factors regulate the expression of E-cadherin. Loss of E-cadherin has been reported to induce epithelial-mesenchymal transition in several cancers. This review highlights recent advances in defining the mechanisms that regulate E-cadherin expression in breast cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology*
  • Cadherins / genetics*
  • Cell Adhesion / genetics
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Transcription, Genetic


  • Cadherins