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Review Article Loss of Function of E-Cadherin in Embryonic Stem Cells and the Relevance to Models of Tumorigenesis

By Lisa Mohamet, Kate Hawkins and Christopher M. Ward

Abstract

Copyright © 2011 Lisa Mohamet et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. E-cadherin is the primary cell adhesion molecule within the epithelium, and loss of this protein is associated with a more aggressive tumour phenotype and poorer patient prognosis in many cancers. Loss of E-cadherin is a defining characteristic of epithelialmesenchymal transition (EMT), a process associated with tumour cell metastasis. We have previously demonstrated an EMT event during embryonic stem (ES) cell differentiation, and that loss of E-cadherin in these cells results in altered growth factor response and changes in cell surface localisation of promigratory molecules. We discuss the implication of loss of E-cadherin in ES cells within the context of cancer stem cells and current models of tumorigenesis. We propose that aberrant E-cadherin expression is a critical contributing factor to neoplasia and the early stages of tumorigenesis in the absence of EMT by altering growth factor response of the cells, resulting in increased proliferation, decreased apoptosis, and acquisition of a stem cell-like phenotype. 1. E-Cadherin Protein Structure and Function Cadherins are a family of calcium ion-dependent cell surface glycoproteins that function in cell-cell adhesion. The cadherin family is divided into classical (Type I) and nonclassical (Type II) subtypes, as well as other categories whic

Year: 2013
OAI identifier: oai:CiteSeerX.psu:10.1.1.292.3765
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