A variety of molecular crosstalks between extracellular matrices and their cell surface receptors in oral carcinomas

我们分析了口腔癌细胞对细胞外基质(ECM)分子的生物合成，如从人腺样囊性癌细胞建立的ACC3，从口腔鳞癌建立的MK-1和ZK-1。这些癌细胞产生基膜相关分子，尤其是基膜型硫酸乙酰肝素蛋白多糖HSPG/perlecan和纤维连接蛋白FN。这两种ECM分子的相对分子质量因细胞类型而异。我们用35S-蛋氨酸标记的细胞和几种寡糖裂解酶的组合进行免疫沉淀，研究了它们之间分子大小变化的分子背景。ACC3细胞产生高分子量的HSPG/FN，这是由于N-和O-连接的寡糖链的选择性剪接和增加而导致较大的蛋白质的结果，尽管对于HSPG核心蛋白的选择性剪接机制还需要更多的研究。类似的，整合素，整合素，受体…更多的是ECM分子，这些细胞表达的分子大小不同。这主要是由于低聚糖的添加。因此，口腔癌细胞之间存在多种ECM分子及其受体的结构。由于ECM分子的大小与细胞的附着能力是平行的，因此认为ECM分子的大小因癌细胞类型的不同而不同，ECM分子与其受体之间的各种分子串扰也应反映在口腔癌的组织结构和肉芽组织的组织重塑过程中。我们还对这些分子在口腔肿瘤和炎症病变中进行了免疫定位。针对这些免疫组织化学实验，我们提出了不同组织中细胞外基质分子的酶前处理指南。这些结果清楚地表明，细胞外基质分子及其受体的分子结构随着细胞类型的不同而不同，这种分子变化应该反映在它们的临床过程中。然而，从目前的研究中还不知道是什么调节了这种分子多样性，以及这些变异是否真的在体外人类癌症组织中发挥了作用。较少

We have analyzed biosynthesis of extracellular matrix(ECM)molecules by oral carcinoma cells, such as ACC3 established from a human adenoid cystic carcinoma cells, MK-1 and ZK-1 established from oral squamous cell carcinomas. These carcinoma cells were shown to produce basement membrane-associated molecules, especially basement membrane type heparan sulfate proteoglycan, HSPG/perlecan, and fibronectin, FN.These two ECM molecules were different in molecular weight with cell types. We examined the molecular background for the variations in molecular size among them, by using immunoprecipitation of 35S-methionin labeled cells with several combinations of oligosaccharide lyases. ACC3 cells produced high molecular weight HSPG/FN, which were resulted from larger proteins due to alternative splicing and addition of N-and O-linked oligosaccharide chains, although more investigations are necessary for the alternative splicing mechanism for HSPG core protein.Similarly, integrins, INTs, receptors … More for ECM molecules, expressed by these cells were different in size. This was mainly due to oligosaccharide additions. Thus, there was a variety of structures of ECM molecules and their receptors among oral carcinoma cells. Since the molecular sizes were parallel with the attachment ability of the cells, it is suggested that the ECM molecular size, which is varied with carcinoma cell types, regulate the biological nature of them.Such a variety of molecular crosstalks between ECM molecules and their receptors should be also reflected to the tissue architecture of oral carcinomas as well as tissue remodeling processes of granulation tissues. We also immunolocalized these molecules in oral neoplastic and inflammatory lesions. In relation to these immunohistochemical experiments, we proposed a guideline for enzymatic pretreatments for ECM molecules in various tissue types.These results clearly indicate that the molecular structures of ECM molecules and their receptors vary with cell types and that the molecular variety should be reflected in their clinical courses. However, it is unknown from the present study what regulates such molecular variety and if these varieties are actually functions in human carcinoma tissues in vitro. Less