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

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.

Automated summary

Loss of E-cadherin is not only linked to cancer metastasis, but also influences cell signaling events and cellular plasticity. This study highlighted the importance of E-cadherin as a global regulator in driving EMT and the metastatic phenotype, inspiring further research in the field.