Ciołczyk-Wierzbicka Dorota, Amoresano Angela, Casbarra Annarita, Hoja-Łukowicz Dorota, Lityńska Anna, Laidler Piotr
Intitute of Medical Biochemistry, Medical College, Jagiellonian University, Kraków, Poland.
Glycoconj J. 2004;20(7-8):483-92. doi: 10.1023/B:GLYC.0000038294.72088.b0.
N-cadherin is calcium-dependent cell adhesion molecule that mediates cell-cell adhesion and also modulates cell migration and tumor invasion. N-cadherin is a heavily glycosylated protein. Many studies have demonstrated that malignant transformation of a number of cell types correlates with changes of cell surface N-linked oligosacharides. We have studied the carbohydrate profile of N-cadherin synthesized in human melanoma cell lines and the effect of this protein and complex N-glycans on in vitro migration of melanoma cells from the primary tumor site--WM35 and from different metastatic sites WM239 (skin), WM9 (lymph node), and A375 (solid tumor). N-cadherin was immunoprecipitated with anti-human N-cadherin polyclonal antibodies. Characterization of its carbohydrate moieties was carried out by SDS-PAGE electrophoresis and blotting, followed by immunochemical identification of the N-cadherin polypeptides and on-blot deglycosylation using PNGase F for glycan release. N-glycans were separated by matrix-assisted laser desorption/ionization mass spectrometry (MALDI MS) and their structures identified by the computer matching of the resulting masses with those derived from a sequence database. The assay of in vitro chemotaxic cell migration was performed using QCM Cell Invasion Assay (Chemicon). N-cadherin from WM35 (primary tumor site) possessed high-mannose and biantennary complex type glycans with alpha2-6 linked sialic acid. N-cadherin from WM239, WM9, and A375 cell lines possessed mostly tri- or tetra-antennary complex type glycans. In addition, N-cadherin from WM9 (lymph node metastatic site) and A375 (solid tumor metastatic site) contained heavily alpha-fucosylated complex type chains with alpha2,3 linked sialic acid. Blocking of N-cadherin-mediated intercellular interaction by N-cadherin-specific antibodies significantly (of about 40%) inhibited migration of melanoma cells. Inhibition of synthesis of complex type N-glycans by swainsonine (mannosidase II inhibitor) led to 50% decrease of cell migration. The results indicated differences between N-cadherin glycans from primary and metastatic sites and confirmed influence of N-cadherin and complex -type N-glycans on in vitro migration of melanoma cells.
N-钙黏蛋白是一种钙依赖性细胞黏附分子,介导细胞间黏附,还可调节细胞迁移和肿瘤侵袭。N-钙黏蛋白是一种高度糖基化的蛋白质。许多研究表明,多种细胞类型的恶性转化与细胞表面N-连接寡糖的变化相关。我们研究了人黑色素瘤细胞系中合成的N-钙黏蛋白的糖谱,以及这种蛋白质和复合N-聚糖对黑色素瘤细胞从原发性肿瘤部位(WM35)和不同转移部位(WM239(皮肤)、WM9(淋巴结)和A375(实体瘤))的体外迁移的影响。用抗人N-钙黏蛋白多克隆抗体免疫沉淀N-钙黏蛋白。通过SDS-PAGE电泳和印迹对其糖部分进行表征,随后对N-钙黏蛋白多肽进行免疫化学鉴定,并使用PNGase F进行印迹上的去糖基化以释放聚糖。通过基质辅助激光解吸/电离质谱(MALDI MS)分离N-聚糖,并通过将所得质量与序列数据库中的质量进行计算机匹配来鉴定其结构。使用QCM细胞侵袭试验(Chemicon)进行体外趋化细胞迁移测定。来自WM35(原发性肿瘤部位)的N-钙黏蛋白具有高甘露糖和带有α2-6连接唾液酸的双天线复合型聚糖。来自WM239、WM9和A375细胞系的N-钙黏蛋白主要具有三天线或四天线复合型聚糖。此外,来自WM9(淋巴结转移部位)和A375(实体瘤转移部位)的N-钙黏蛋白含有带有α2,3连接唾液酸的高度α-岩藻糖基化复合型链。用N-钙黏蛋白特异性抗体阻断N-钙黏蛋白介导的细胞间相互作用可显著(约40%)抑制黑色素瘤细胞的迁移。用苦马豆素(甘露糖苷酶II抑制剂)抑制复合型N-聚糖的合成导致细胞迁移减少50%。结果表明原发性和转移部位的N-钙黏蛋白聚糖之间存在差异,并证实了N-钙黏蛋白和复合型N-聚糖对黑色素瘤细胞体外迁移的影响。