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

O Schmalhofer, S Brabletz, T Brabletz - Cancer and Metastasis Reviews, 2009 - Springer
O Schmalhofer, S Brabletz, T Brabletz
Cancer and Metastasis Reviews, 2009Springer
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, eg 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 …
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 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.
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