Department of Life Sciences, Division of Molecular Life Sciences and Center for Cell Signaling Research, Ewha Womans University, Seoul 120-725, Republic of Korea.
Biochem Biophys Res Commun. 2013 Feb 15;431(3):415-20. doi: 10.1016/j.bbrc.2012.12.155. Epub 2013 Jan 16.
The cell surface heparan sulfate proteoglycan, syndecan-2, is known to play an important role in the tumorigenic activity of colon cancer cells, but the function of its extracellular domain is not yet clear. Cell spreading assays showed that HCT116 human colon cancer cells attached and spread better on fibronectin compared to the other tested extracellular matrixes (ECMs). Notably, syndecan-2 overexpression enhanced the spreading of HCT116 cells on fibronectin, and the opposite effects were observed when syndecan-2 expression was reduced. In addition, an oligomerization-defective syndecan-2 mutant failed to increase cell-ECM interactions and adhesion-related syndecan-2 functions, including migration. Furthermore, analyses using a microfabricated post array detector system revealed that syndecan-2, but not the oligomerization-defective mutant, enhanced the interaction affinity of HCT116 cells on fibronectin. Taken together, these results suggest that the extracellular domain of syndecan-2 regulates the interaction of HCT116 human colon carcinoma cells with fibronectin.
细胞表面硫酸乙酰肝素蛋白聚糖，即黏附素-2，其在结肠癌肿瘤细胞的致瘤活性中起着重要作用，但它的细胞外结构域的功能尚不清楚。细胞铺展实验表明，与其他测试的细胞外基质（ECM）相比，HCT116 人结肠癌细胞在纤连蛋白上附着和铺展得更好。值得注意的是，黏附素-2 的过表达增强了 HCT116 细胞在纤连蛋白上的铺展，而当黏附素-2 的表达减少时则观察到相反的效果。此外，寡聚缺陷黏附素-2 突变体不能增加细胞与细胞外基质的相互作用和黏附相关的黏附素-2 功能，包括迁移。此外，使用微制造的柱阵列检测器系统进行的分析表明，黏附素-2 而非寡聚缺陷突变体增强了 HCT116 细胞在纤连蛋白上的相互作用亲和力。总之，这些结果表明黏附素-2 的细胞外结构域调节了 HCT116 人结肠癌细胞与纤连蛋白的相互作用。
