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

来源 :现代肿瘤医学 | 被引量 : 0次 | 上传用户:benben0070
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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。 OBJECTIVE: To compare the tumorigenicity and the expression of vascular endothelial growth factor (VEGF) and VEGFR1 and VEGFR2 in xenograft tumor in nude mice before and after transfection with α1,2-fucosyltransferase gene. Methods: The stable and highly expressed human ovarian cancer cell line RMG-IH and the transfected cell line RMG-I were established by established Lewisy antigen. Cell lines were transplanted into nude mice before and after transfection , Observed two groups of tumor growth. Animals were sacrificed on the fifth week, the weight of the transplanted tumor was measured, and the expression of VEGF, VEGFR1 and VEGFR2 in tumor tissue was detected by immunohistochemical method. RESULTS: Tumor formation was observed in both transfection and untransfected nude mice, but the time to tumor formation in the transfection group (5.2 ± 0.8 days) was earlier than that in the untransfected group (8.8 ± 1.3 days) Tumor weight and volume were significantly increased compared with untransfected group (P <0.05). Transfection group nude mice transplantation tumor VEGF and VEGFR2 expression was significantly higher than the untransfected group (P all <0.05). Conclusion: High expression of Lewisy antigen can increase the in vivo tumorigenicity of RMG-I cells and up-regulate the expression of VEGF and VEGFR2 in nude mice. It is suggested that Lewisy antigen can increase the malignant degree of cancer cells, and this effect is closely related to the increase of VEGF and VEGFR2 expression.
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