E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer
- First Online:
- Cite this article as:
- Schmalhofer, O., Brabletz, S. & Brabletz, T. Cancer Metastasis Rev (2009) 28: 151. doi:10.1007/s10555-008-9179-y
- 3.7k Downloads
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 β-catenin. In addition to an accumulation of cancer stem cells, nuclear β-catenin induces a gene expression pattern favoring tumor invasion, and mounting evidence indicates multiple reciprocal interactions of E-cadherin and β-catenin with EMT-inducing transcriptional repressors to stabilize an invasive mesenchymal phenotype of epithelial tumor cells.