Lewis y高表达对人卵巢癌RMG-I细胞裸鼠体内致瘤性及移植瘤VEGF和VEGFR表达的影响

目的：比较α1,2岩藻糖转移酶基因转染前后卵巢癌细胞株RMG-I的裸鼠体内致瘤性及移植瘤组织血管内皮生长因子及其受体VEGFR1和VEGFR2表达的变化。方法：利用已建立的Lewisy抗原稳定高表达卵巢癌细胞株RMG-I-H及转染前细胞株RMG-I为细胞模型,将转染前后细胞株种植裸鼠皮下建立人卵巢癌裸鼠移植瘤模型,观察两组肿瘤生长情况。第5周处死动物,测量移植瘤重量,免疫组织化学方法检测肿瘤组织VEGF及VEGFR1、VEGFR2的表达。结果：转染组及未转染组裸鼠均有荷瘤形成,但转染组的成瘤时间（5.2±0.8d）早于未转染组（8.8±1.3d）,且转染组的瘤重和体积与未转染组相比均明显增加（P〈0.05）。转染组裸鼠移植瘤组织VEGF及VEGFR2表达量明显高于未转染组（P均〈0.05）。结论：Lewisy抗原高表达能增加卵巢癌RMG-I细胞的体内致瘤性,上调裸鼠移植瘤VEGF及VEGFR2的表达。提示Lewisy抗原能提高癌细胞的恶性程度,且该作用与VEGF及VEGFR2表达增高关系密切。

Influence of Lewis y high expression on tumorigenicity and expression of VEGF and VEGF receptor in ovarian carcinoma-derived RMG-I cells in nude mice

Objective：To compare the tumorigenicity in vivo of cells with or without transfection of α1,2-fucosyltransferase gene and changes of expression of vascular endothelial growth factor and vascular endothelial growth factor receptors VEGFR1 and VEGFR2 in transplanted tumor tissue.Methods：Nude mice were subcutaneously injected with RMG-I-H cells that stably express Lewis y antigen at high levels,RMG-I cells as control.After five weeks,animals were killed.Tumorigenicity was monitored and compared among the animals.Expression of VEGF,VEGFR1 and VEGFR2 in tumor tissue was detected by immunohistochemistry.Results：Nude mice in both groups had subcutaneous tumor formation,but the time of tumor formation （5.2 ± 0.8 d） in transfected group was earlier than that of non-transfected group （8.8 ± 1.3 d）,and the weight and volume of tumors in transfected group were also significantly increased compared with non-transfected group （P〈0.05）.Expression of VEGF and VEGFR2 in transplanted tumor tissue in transfection group was significantly higher than that in non-transfected group （P〈0.05）.Conclusion：Lewis y antigen high expression can enhance the tumorigenicity in vivo of RMG-I cells and up-regulate the expression of VEGF and VEGFR2 in transplanted tumor tissue.These results suggest that Lewis y antigen can enhance the degree of malignancy of cancer cells,and this is closely related to the high expression of VEGF and VEGFR2.