Analysis of E-Cadherin (Human) by ELISA (CAT#: STEM-MB-0773-LGZ)

Introduction

Loss of E-cadherin expression is a hallmark of epithelial-mesenchymal transition (EMT) and is associated with an increased risk of cancer metastasis. However, it remains unclear whether E-cadherin and its downstream signaling pathways are functionally involved in driving EMT and pro-metastatic phenotypes. In 2008, Onder et al. found in a study that loss of E-cadherin not only helps tumor cells to separate from each other by disrupting the connection between cells, but also induces intracellular signaling events to produce mesenchymal cell state and metastatic phenotype. This study establishes E-cadherin as an important global regulator and not just a marker of EMT. This discovery inspired further research over the next decade, greatly improving our understanding of E-cadherin and its diverse functions, and more broadly, cellular plasticity at different stages and in the context of cancer metastasis.