Journal
JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA
Volume 12, Issue 2-3, Pages 127-133Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10911-007-9044-6
Keywords
adhesion; metastasis; breast cancer; signaling; invasion
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Funding
- NCI NIH HHS [R01 CA90872] Funding Source: Medline
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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.
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