Abstract
The cadherin family of adhesion molecules regulates cell-cell interactions during development and in tissues. The prototypical cadherin, E-cadherin, is responsible for maintaining interactions of epithelial cells and is frequently downregulated during tumor progression. N-cadherin, normally found in fibroblasts and neural cells, can be upregulated during tumor progression and can increase the invasiveness of tumor cells. The proinvasive effects of N-cadherin expression in tumor cells result from two possible mechanisms: promotion of tumor cell interactions with the N-cadherin-expressing microenvironment, or enhancement of signaling via the fibroblast growth factor receptor. The downregulation of E-cadherin and the upregulation of N-cadherin in tumors may be a result of an epithelial to mesenchymal transformation (EMT) of tumor cells, which is notoriously difficult to detect in vivo. Double labeling of individual tumors with specific E- and N-cadherin antibodies suggests that EMT can occur heterogeneously and/or transiently within an invasive tumor. © Springer Science+Business Media, LLC 2007.
Original language | English |
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Pages (from-to) | 127-133 |
Number of pages | 6 |
Journal | Journal of Mammary Gland Biology and Neoplasia |
Volume | 12 |
Issue number | 2-3 |
DOIs | |
Publication status | Published - Sept 2007 |
Keywords
- Adhesion
- Breast cancer
- Invasion
- Metastasis
- Signaling