@article{204171,
  keywords = {Humans, signal transduction, Neoplasms, Epithelial-Mesenchymal Transition, Cadherins},
  author = {Cao Fang and Yibin Kang},
  title = {E-Cadherin: Context-Dependent Functions of a Quintessential Epithelial Marker in Metastasis},
  abstract = {<p>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..</p>
},
  year = {2021},
  journal = {Cancer Res},
  volume = {81},
  pages = {5800-5802},
  month = {12/2021},
  issn = {1538-7445},
  doi = {10.1158/0008-5472.CAN-21-3302},
  language = {eng},
}