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

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

Author information

1
Department of Visceral Surgery, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.

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.

PMID:
19153669
DOI:
10.1007/s10555-008-9179-y
[Indexed for MEDLINE]

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