Department of Molecular Biology, Princeton University, Princeton, New Jersey.
Ludwig Institute for Cancer Research Princeton Branch, Princeton University, Princeton, New Jersey.
Cancer Res. 2021 Dec 1;81(23):5800-5802. doi: 10.1158/0008-5472.CAN-21-3302.
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..
E-钙黏蛋白表达的丧失已被公认为上皮-间充质转化 (EMT) 的标志，这与癌症转移的风险增加有关。然而，尚不清楚 E-钙黏蛋白及其下游信号通路是否在功能上参与驱动 EMT 和促转移表型。2008 年，Onder 及其同事的一项研究发现，E-钙黏蛋白的丧失不仅通过破坏细胞-细胞连接帮助肿瘤细胞彼此分离，还引发细胞内信号事件，赋予间充质细胞状态和转移表型。这项研究确立了 E-钙黏蛋白作为 EMT 的一个重要的全局调节剂，而不仅仅是一个标志物。这一发现激发了随后十年的进一步研究，极大地加深了我们对 E-钙黏蛋白及其多种功能的理解，更广泛地说，还加深了我们对癌症转移不同阶段和不同环境下细胞可塑性的理解。
