中文摘要：

细胞表面的糖链参与信号分子识别、细胞间的识别、黏附等多种生物学功能，在肿瘤的侵袭和转移过程中也扮演重要角色。当细胞癌变时，细胞表面的糖链通常异常表达，其原因主要是合成糖链的糖基转移酶表达水平变化。该实验通过流式细胞术发现CML细胞株K562表面T抗原、唾液酸化的T抗原和多聚乳糖胺的表达水平~tMeg—01细胞高；而RT-PCR结果显示两细胞株间ppGalNAcT2、C1GalTl和ST6GalNAcl种糖基转移酶基因的mRNA的表达水平没有差异性，但K562细胞中ST3Gall、B3GnT8和ST6GalNAc4的mRNA表达水平lzLMeg．01高；并且发现伊马替尼能抑制K562细胞表面多聚乳糖胺及合成多聚乳糖胺的B3GnT8的表达。由于K562细胞是由转移至胸腔的CML细胞建系而来的，因此推测细胞表面T抗原、唾液酸化的T抗原和多聚乳糖胺在CML的侵袭转移过程中可能具有一定的作用，而伊马替尼处理K562细胞后对细胞表面糖链结构的改变其分子机制值得进一步研究。

英文摘要：

Cell surface glycans involved in signaling recognition,cell-cell recognition,cell adhesion and other biological functions,and also play an important role in tumor invasion and metastasis.When cell carcinogenesis,the cell surface sugar chains usually take on abnormal expression,which was mainly due to the variation of glycosyltransferases expression.The experiment found that T antigen,sialylated T antigen and poly-galactosamine on K562 cells surface expression levels were higher than Meg-01 cells;while the RT-PCR results showed that mRNA expression levels of ppGalNAcT2,C1GalT1 and ST6GalNAcl did not differ in two cell lines,but mRNA expression levels of ST3Gall,~3GnT8 and ST6GalNAc4 in K562 cells were higher than Meg-01 .The experiment also discovered that imatinib can inhibit poly-lactosamine on K562 cell surface and 133GnT8 synthesis of poly- lactosamine.Since K562 cells stem from CML cells transferred to the chest cavity, it suggests that T antigen, sialylated T antigen and poly-galactosamine have some effect in the process of invasion and metastasis of CML,but the specific mechanisms of the K562 cell surface sugar chain structure variation after imatinib treating deserve further study.