Agiostratidou Georgia, Hulit James, Phillips Greg R, Hazan Rachel B
Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
J Mammary Gland Biol Neoplasia. 2007 Sep;12(2-3):127-33. doi: 10.1007/s10911-007-9044-6.
The cadherin family of adhesion molecules regulates cell-cell interactions during development and in tissues. The prototypical cadherin, E-cadherin, is responsible for maintaining interactions of epithelial cells and is frequently downregulated during tumor progression. N-cadherin, normally found in fibroblasts and neural cells, can be upregulated during tumor progression and can increase the invasiveness of tumor cells. The proinvasive effects of N-cadherin expression in tumor cells result from two possible mechanisms: promotion of tumor cell interactions with the N-cadherin-expressing microenvironment, or enhancement of signaling via the fibroblast growth factor receptor. The downregulation of E-cadherin and the upregulation of N-cadherin in tumors may be a result of an epithelial to mesenchymal transformation (EMT) of tumor cells, which is notoriously difficult to detect in vivo. Double labeling of individual tumors with specific E- and N-cadherin antibodies suggests that EMT can occur heterogeneously and/or transiently within an invasive tumor.
钙黏蛋白家族的黏附分子在发育过程和组织中调节细胞间相互作用。典型的钙黏蛋白E-钙黏蛋白负责维持上皮细胞间的相互作用，在肿瘤进展过程中常被下调。N-钙黏蛋白通常存在于成纤维细胞和神经细胞中，在肿瘤进展过程中可被上调，并可增加肿瘤细胞的侵袭性。肿瘤细胞中N-钙黏蛋白表达的促侵袭作用源于两种可能的机制：促进肿瘤细胞与表达N-钙黏蛋白的微环境相互作用，或增强成纤维细胞生长因子受体介导的信号传导。肿瘤中E-钙黏蛋白的下调和N-钙黏蛋白的上调可能是肿瘤细胞上皮-间质转化（EMT）的结果，而这种转化在体内很难检测到。用特异性E-钙黏蛋白和N-钙黏蛋白抗体对单个肿瘤进行双重标记表明，EMT可在侵袭性肿瘤内异质性和/或短暂性地发生。
