机构地区:[1]上海医科大学卫生部糖复合物重点实验室,生物化学教研室,上海200032 [2]上海医科大学中山医院肝癌研究所,上海200032
出 处:《生物化学与生物物理学报》2000年第2期115-120,共6页
基 金:国家自然科学基金资助项目,No.39630080;"九五"国家医学科技攻关基金资助项目,No.969060115;上海市教委重点学科基础资助项目
摘 要:为了测定人原发性肝癌中Lewis抗原和α1,3岩藻糖转移酶 (FucT)亚型的表达 ,及其与癌栓形成和转移抑制基因nm2 3 H1表达的关系 ,用免疫组化法测Lewis抗原 ,用Northern印迹法测FucT和nm2 3 H1的mRNA。结果表明 ,肝癌组织中SLex、Lex、SDLex、SLea4种Lewis抗原表达的阳性率均在 80 %左右。其中SLex 表达较多 ,Lex 和SLea 较少 ,SDLex 极少。但在癌旁组织中 ,4种Lewis抗原均不表达。肝癌组织中α1,3FucT III/VImRNA的转录水平高于癌旁肝组织 ,特别在有癌栓病人的肝癌组织中更显著增高 ;而在癌旁组织中 ,不论病人有、无癌栓存在 ,α1,3FucT III/VI的表达几乎没有区别。但癌组织与癌旁组织中α1,3FucT VII仅有少量表达。另外 ,有癌栓病人的癌组织中 ,转移抑制基因nm2 3 H1的表达明显低于无癌栓病人的癌组织及癌旁组织 ,且与α1,3FucT III/VI的表达呈负相关。肝癌组织中α1,3FucT III/VI及其产物SLex 的表达与癌栓形成 (转移倾向 )有关。nm2 3 H1的作用机制之一可能是通过下调α1,3FucT及SLex 来实现其抑制肝癌转移的作用。In order to study the expression of Lewis antigens and the subtypes of α1,3 fucosyltransferase (α1,3 FucT) in human primary liver cancer, and their relations with the cancer cell embolus formation, as well as the expression of nm 23 H1, a metastatic suppressor gene, Lewis antigens were detected with immunohistochemical method, and the mRNA of α1,3 FucTs and nm 23 H1 were determined with Northern blot. Results showed that the positive rates of the expression of four Lewis antigens, sialyl Lewis X(SLe x), Lewis X(Le x), sialyl dimeric Lewis X(SDLe x) and sialyl Lewis A(SLe a), in human primary liver cancer were about 80%. The expression of SLe x was rather higher, Le x and SLe a were lower, but the expression of SDLe x was only in trace amount. The four Lewis antigens were not expressed in the liver regions adjacent to the cancer tissues. The transcriptional level of α1,3 FucT III/VI mRNA in cancer tissues was higher than that in the adjacent regions, especially in the cancer tissues of patients with portal vein cancer cell embolus(CCE). However, the expression of α1,3 FucT III/VI mRNA was not different in the adjacent regions in spite of the presence or absence of CCE in the patients. In contrast, the expression of α1,3 FucT VII was rather lower and identical to each other both in cancer tissues and adjacent regions. In addition, it was found that the expression of nm 23 H1, a metastasis suppressor gene, was markedly lower in the cancer tissues of patients with CCE than that in the non CCE patients and the adjacent regions. Furthermore, the expression of nm 23 H1 was negatively related to the expression of α1,3 FucT III/VI. These results indicated that the expression of α1,3 FucT III/VI and its product SLe x were correlated with CCE (metastatic potential), and the down regulation of α1,3 FucT III/VI and SLe x may be one of the mechanisms of nm23 H1 to inhibit liver cancer metastasis.
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