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作 者:刘飞[1] 刘爱华[1] 巨同忠[1] 陈惠黎[1]
机构地区:[1]卫生部糖复合物重点实验室-上海医科大学基础医学院生物化学教研室
出 处:《上海医科大学学报》1999年第2期122-124,共3页Journal of Fudan University(Medical Science)
基 金:国家自然科学基金
摘 要:目的研究肝癌细胞和白血病细胞诱导分化时α1,6岩藻糖转移酶(α1,6FucT)的改变。方法采用生物素标记受体糖链,用LCA亲和层析柱分离被核心岩藻糖化的产物,并以辣根过氧化酶(HRP)标记的亲和素与柱上的产物结合,最后测定洗脱液中HRP的活力,可代表α1,6FucT活力。结果全反式维甲酸(ATRA)或双丁酰环磷腺苷(db-cAMP)诱导7721人肝癌细胞分化后,α1,6-FucT活力均降低。ATRA或正丁酸使HL-60早幼粒白细胞分化成粒细胞,佛波醇-12-豆蔻酸-13乙酸酯(PMA)使HL-60细胞分化成单核细胞时都使α1,6FucT活力下降,而用二甲亚砜(DMSO)或神经节苷酯GM3使HL-60细胞分化成粒细胞或单核细胞时,α1,6FucT活力则上升。结论α1,6-FucT活力下降是肝癌细胞的分化指标,但和HL-60细胞的分化关系不大。Purpose To study the changes of the activity α1,6fucosyltransferase(α1,6FucT) during the induced differentiation of hepatocarcinoma cells and leukemia cells. Methods Biotinlabeled acceptor Nglycan was used as substrate.The corefucosylated product was isolated from substrate using LCA lectin affinity chromatographic column.After HRPavidin conjugate was bound to the biotinylated product on the column,the HRP avidin biotinylated product was eluted from the column and the activity of HRP was determined as a measure of α 1,6FucT activity. Results α 1,6FucT activity was decreased in the induced differentiation of human hepatocarcinoma cell line 7721 by both ATRA and db cAMP.α1,6FucT was also decreased during the induced differentiation of HL60 cells to myelocyte by ATRA or n butysic acid,as well as to monocyte by PMA.Whereas,the enzyme activity was increased when HL60 cells were induced to differentiate to myelocyte by DMSO and to monocyte by ganglioside GM 3. Conclusions The decrease of α 1,6FucT activity is an index of differentiation for hepatocarcinoma cells,but not for HL60 cells.
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