Jeanes A, Gottardi C J, Yap A S
1Division of Molecular Cell Biology, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland, Australia.
Oncogene. 2008 Nov 24;27(55):6920-9. doi: 10.1038/onc.2008.343.
It has long been recognized that the cell-cell adhesion receptor, E-cadherin, is an important determinant of tumor progression, serving as a suppressor of invasion and metastasis in many contexts. Yet how the loss of E-cadherin function promotes tumor progression is poorly understood. In this review, we focus on three potential underlying mechanisms: the capacity of E-cadherin to regulate beta-catenin signaling in the canonical Wnt pathway; its potential to inhibit mitogenic signaling through growth factor receptors and the possible links between cadherins and the molecular determinants of epithelial polarity. Each of these potential mechanisms provides insights into the complexity that is likely responsible for the tumor-suppressive action of E-cadherin.
长期以来，人们一直认识到细胞间粘附受体E-钙粘蛋白是肿瘤进展的重要决定因素，在许多情况下作为侵袭和转移的抑制因子。然而，E-钙粘蛋白功能丧失如何促进肿瘤进展却知之甚少。在这篇综述中，我们关注三个潜在的潜在机制：E-钙粘蛋白在经典Wnt通路中调节β-连环蛋白信号传导的能力；其通过生长因子受体抑制有丝分裂信号传导的潜力以及钙粘蛋白与上皮极性分子决定因素之间的可能联系。这些潜在机制中的每一个都为可能导致E-钙粘蛋白肿瘤抑制作用的复杂性提供了见解。
