Loss of E-cadherin expression has been well known as a hallmark of epithelial-mesenchymal transition (EMT), which is linked to increased risk of cancermetastasis. However, itwas less clear whether E-cadherin and its downstream signaling pathways are functionally involved in drivingEMTandthe prometastatic phenotype.Astudy by Onder and colleagues in 2008 discovered that E-cadherin loss not only helps tumor cells detach fromeach 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.
|Original language||English (US)|
|Number of pages||3|
|State||Published - Dec 1 2021|
All Science Journal Classification (ASJC) codes
- Cancer Research