application of ganglioside GM3 and glycosyltransforase for bladder cancer treatment

1.人膀胱肿瘤中糖脂表达的变化侵袭性肿瘤时，GM3在乳头状、浅表性肿瘤中大量积累最为显著。外源添加浓度为10 ~ 100mug/ml的GM3均能抑制人移行细胞癌T-24和KK47的体外侵袭活性。膀胱肿瘤糖基转移酶活性研究。g3、GM3、GD3合成酶活性的改变与浅表肿瘤中GM3的积累一致。BBN诱导大鼠膀胱肿瘤中糖脂表达的变化。我们强调内镜下观察BBN诱导大鼠膀胱肿瘤规范化的重要性。糖脂在肿瘤发生过程中的表达变化尚不清楚。Brefeldin改变人膀胱肿瘤细胞中神经节苷脂的表达模式，抑制其体外侵袭活性。观察Brefeldin A对T24、YTS-1、KK47、YTS-3和HCV-29的神经节苷元组成、生长活性和侵袭活性的影响。Brefeldin A降低了sialylLe^x的表达，增加了GM3的表达。Brefeldin A在低浓度下抑制细胞的侵袭活性。局部给药GM3对小鼠MBT-2肿瘤的抗肿瘤作用。局部注射GM3可抑制皮下接种MBT-2的侵袭和生长，浓度分别为10和100mug/ml。合成GM3的alpha2,3唾液基转移酶的C-DNA尚未克隆。因此，通过转染alpha2,3唾液基转移酶改变肿瘤细胞表型来控制其侵袭活性仍然是不可能的。

1.Glycolipid expression chages in human bladder tumorMassive GM3 accumulation in papillary, superficial tumor was the most conspicuous change against invasive tumors. The in vitro invasion activity of human transitional cell carcinoma, T-24 and KK47 were both inhibited by exogeneously added GM3 at the concentration of 10-100mug/ml.2.Glycosyltransferase activity in human bladder tumor sample.The altered activities of Gb3, GM3, GD3 synthetases were consistent with GM3 accumulation in supericial tumors.3.Glycolipid expression changes in BBN induced rat bladder tumor.We emphasized the importance of standardization of the BBN induced rat bladder tumor by endoscopic observation. The glycolipid expression changes during tumor development remained unknown.4.Brefeldin A altered ganglioside expression pattern in human bladder tumor cells and inhibits their in vitro invasion activity.T24, YTS-1, KK47, YTS-3 and HCV-29 were assessed about their alteration in ganglioside composition, growth activity and invasion activity affected by Brefeldin A administration. Brefeldin A reduced sialylLe^x expression and increased GM3 expression. Brefeldin A inhibited the invasion activities of the cells at a low concentration.5.Anti-tumor effect of locally administered GM3 on mouse MBT-2 tumor.Locally injected GM3 inhibited invasion and growth of the subcutaneously inoculated MBT-2 at the concentration of 10 and 100mug/ml. The C-DNA of alpha2,3 sialyltransferase that synthesize GM3 has not yet been cloned. Thus, it remained impossible to control the invasion activity through the altered tumor cell phenotype by alpha2,3 sialyltransferase transfection.