Iida J, Meijne A M, Knutson J R, Furcht L T, McCarthy J B
University of Minnesota, Department of Laboratory Medicine and Pathology, Minneapolis, USA.
Semin Cancer Biol. 1996 Jun;7(3):155-62. doi: 10.1006/scbi.1996.0021.
Tumor cell invasion and metastasis is highly dependent on dynamic changes in the adhesion and migration of transformed and malignant cells. As with normal cell adhesion, the adhesion of tumor cells influences their cytoskeletal organization, activation of signal transduction pathways within the cell, and nuclear events leading to changes in mRNA transcription and protein synthesis. Furthermore, as tumor cells invade the circulation, they adhere to activated endothelial cells at sites within the vasculature during arrest and extravasation. Studies in the area of tumor cell adhesion and migration have demonstrated that the recognition of extracellular matrix ligands, or adhesion promoting ligands expressed on neighboring cells (i.e. counter-receptors), involves complex molecular recognition mechanisms. The complexity arises, in part, from the multiple recognition sites that are present within adhesion promoting ligands. Some of these structures within ECM components act by binding integrins, whereas others bind additional receptors such as cell surface proteoglycans. In this sense, adhesion promoting ligands may be considered as informational arrays, that function to modulate cell phenotype by engaging specific combinations of adhesion receptors on the cell surface. Understanding the mechanism(s) by which these receptor 'cluster' modify cell adhesion, motility and growth may lead to novel therapeutic strategies to control tumor cell invasion and metastasis formation. This review will highlight the role that cell surface chondroitin sulfate proteoglycans may play in modulating tumor cell adhesion, migration and invasion, with an emphasis on the relationship between cell surface chondroitin sulfate proteoglycans and integrins.
肿瘤细胞的侵袭和转移高度依赖于转化细胞和恶性细胞黏附与迁移的动态变化。与正常细胞黏附一样，肿瘤细胞的黏附会影响其细胞骨架组织、细胞内信号转导通路的激活以及导致mRNA转录和蛋白质合成变化的核事件。此外，当肿瘤细胞侵入循环系统时，它们在血管内的滞留和外渗部位会黏附于活化的内皮细胞。肿瘤细胞黏附与迁移领域的研究表明，细胞外基质配体或相邻细胞上表达的促进黏附配体（即反受体）的识别涉及复杂的分子识别机制。这种复杂性部分源于促进黏附配体中存在的多个识别位点。细胞外基质成分中的一些结构通过结合整合素来发挥作用，而其他结构则结合其他受体，如细胞表面蛋白聚糖。从这个意义上说，促进黏附配体可被视为信息阵列，其功能是通过与细胞表面特定组合的黏附受体结合来调节细胞表型。了解这些受体“簇”改变细胞黏附、运动和生长的机制可能会带来控制肿瘤细胞侵袭和转移形成的新治疗策略。本综述将重点阐述细胞表面硫酸软骨素蛋白聚糖在调节肿瘤细胞黏附、迁移和侵袭中可能发挥的作用，重点关注细胞表面硫酸软骨素蛋白聚糖与整合素之间的关系。
