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1 May 2010
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Cover Image
Cover Image
Schematic depiction of how N-cadherin, a mesenchymal cell-cell adhesion molecule upregulated during malignant tumor progression, may mediate pro-invasive signaling. First, cell-cell adhesion to N-cadherin–expressing cells of the stroma. Second, binding and activation of FGF receptors (FGFR), which results in FGFR signaling and the promotion of cell survival, migration, and invasion. Third, cleavage and shedding of the extracellular domain of N-cadherin by ADAM metallopeptidase domain 10 (ADAM10). Shedded N-cadherin may neutralize N-cadherin–mediated cell-cell adhesion and/or stimulate FGFR signaling on neighboring cells. Fourth, cleavage of N-cadherin by γ-secretase results in the translocation of the C-terminal fragment of N-cadherin (CTF2) to the nucleus, where it binds CREB-binding protein (CBP), induces its degradation and thus modulates expression. For further details, please see Yilmaz and Christofori on page 629 in this issue.Close Modal - PDF Icon PDF LinkTable of Contents
ISSN 1541-7786
EISSN 1557-3125
Highlights
Subject Review
Angiogenesis, Metastasis, and the Cellular Microenvironment
Cancer Genes and Genomics
Cell Cycle, Cell Death, and Senescence
Signaling and Regulation
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