钙粘蛋白
上皮-间质转换
转移
生物
背景(考古学)
表型
调节器
癌细胞
细胞生物学
癌症
癌症研究
神经科学
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2021-12-01
卷期号:81 (23): 5800-5802
被引量:5
标识
DOI:10.1158/0008-5472.can-21-3302
摘要
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.See related article by Onder and colleagues, Cancer Res 2008;68:3645-54.
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