Journal
CANCER AND METASTASIS REVIEWS
Volume 28, Issue 1-2, Pages 151-166Publisher
SPRINGER
DOI: 10.1007/s10555-008-9179-y
Keywords
E-cadherin; EMT; ZEB1; Cancer; Invasion; Feedback/forward loop
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Funding
- EU MCSC [037297]
- DFG [BR 1399/4-3]
- Deutsche Krebshilfe [106958]
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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.
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