E-Cadherin: Context-Dependent Functions of a Quintessential Epithelial Marker in Metastasis
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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Dec 01, 2021
- Source ID
- 10.1158/0008-5472.can-21-3302
Entities
People
- Cao Fang
- Yibin Kang
Organizations
- American Cancer Society
- Brewster Place
- China Scholarship Council
- Ludwig Institute for Cancer Research
- National Institutes of Health
- Princeton University
- Susan G. Komen for the Cure
- The Breast Cancer Research Foundation
- United States Department of Defense