Journal
ONCOGENE
Volume 27, Issue 55, Pages 6920-6929Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2008.343
Keywords
E-cadherin; beta-catenin; Wnt; growth factor receptor; cell polarity; metastasis
Funding
- National Health and Medical Research Council of Australia
- NIH [GM076561]
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It has long been recognized that the cell-cell adhesion receptor, E-cadherin, is an important determinant of tumor progression, serving as a suppressor of invasion and metastasis in many contexts. Yet how the loss of E-cadherin function promotes tumor progression is poorly understood. In this review, we focus on three potential underlying mechanisms: the capacity of E-cadherin to regulate beta-catenin signaling in the canonical Wnt pathway; its potential to inhibit mitogenic signaling through growth factor receptors and the possible links between cadherins and the molecular determinants of epithelial polarity. Each of these potential mechanisms provides insights into the complexity that is likely responsible for the tumor-suppressive action of E-cadherin.
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