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E-Cadherin: Context-Dependent Functions of a Quintessential Epithelial Marker in Metastasis.

Authors
  • Fang, Cao1, 2
  • Kang, Yibin3, 2
  • 1 Department of Molecular Biology, Princeton University, Princeton, New Jersey. , (Jersey)
  • 2 Ludwig Institute for Cancer Research Princeton Branch, Princeton University, Princeton, New Jersey. , (Jersey)
  • 3 Department of Molecular Biology, Princeton University, Princeton, New Jersey. [email protected] , (Jersey)
Type
Published Article
Journal
Cancer Research
Publisher
American Association for Cancer Research
Publication Date
Dec 01, 2021
Volume
81
Issue
23
Pages
5800–5802
Identifiers
DOI: 10.1158/0008-5472.CAN-21-3302
PMID: 34853039
Source
Medline
Language
English
License
Unknown

Abstract

Loss of E-cadherin expression has been well known as a hallmark of epithelial-mesenchymal transition (EMT), which is linked to increased risk of cancer metastasis. However, it was less clear whether E-cadherin and its downstream signaling pathways are functionally involved in driving EMT and the prometastatic phenotype. A study by Onder and colleagues in 2008 discovered that E-cadherin loss not only helps tumor cells detach from each other by breaking down cell-cell junctions but also elicits intracellular signaling events to confer a mesenchymal cell state and metastatic phenotype. This study established E-cadherin as an important global regulator, rather than just a marker, of EMT. The discovery inspired further investigation in the following decade that significantly deepened our understanding of E-cadherin and its diverse functions and more broadly of cellular plasticity in different stages and contexts of cancer metastasis.See related article by Onder and colleagues, Cancer Res 2008;68:3645-54. ©2021 American Association for Cancer Research.

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