VEGF／KDR双位点抑制诱导膀胱癌细胞凋亡和丝裂霉素C化疗增效的实验研究  

Experimental study of VEGF/KDR double sites inhibition induced apoptosis in bladder carcinoma and the increased chemotherapy effect of mitomycin C

作　　者：刘禄成[1] 韩艳君[2] 魏巍[1] 李然伟[1] 王颂[1] 

机构地区：[1]吉林大学第二医院泌尿外科,吉林长春130041 [2]吉林大学第二医院手术室

出　　处：《中国老年学杂志》2008年第1期5-7,共3页Chinese Journal of Gerontology

基　　金：国家自然科学基金资助项目(30571857)

摘　　要：目的观察针对VEGF/KDR双位点抑制诱导膀胱癌T24细胞凋亡以及对联合应用细胞毒药物丝裂霉素C(MMC)的增效作用。方法将针对血管内皮生长因子(VEGF)的VEGFsiRNA和VEGF受体2(KDR)的可溶性受体(sKDR)表达质粒共转染T24细胞和在其中加入MMC的细胞悬液分别汁射到裸鼠背部皮下,观察两者对裸鼠膀胱痛生长的影响。结果两种制剂均能在不同程度上诱导膀胱癌细胞凋亡,抑制癌细胞增殖,从而延缓甚至遏制肿瘤生长。但加入MMC组作用更显著,效果更好,两组比较,差异具有统计学意义(P<0.05)。结论VEGFsiRNA和sKDR通过双重途径有效抑制VEGF的生物活性,使其促肿瘤血管生成的能力明显降低,诱导细胞凋亡的作用显著提高。在辅以MMC后这种作用效果进一步加强。因此推测,抗VEGF/KDR基因的双位点靶向治疗与肿瘤化疗的结合可能是一个具有诱人前景和巨人潜力的膀胱癌治疗方案。Objective To observe the effect of VEGF/KDR double sites inhibition induced T24 apoptosis and increased chemothera- peutic effect with cytotoxic drug mitomycin C （MMC）. Methods Cell suspension of T24 cells transfected with soluble KDR （sKDR） of VEGF siRNA and VEGF receptor 2 （KDR） and cell suspension added with MMC were subcutaneouly injected into athymic mouse back to observe their effect on angiogenesis in bladder carcinoma. Results Two preparations induced apoptosis in bladder carcinoma and inhibited carcinoma cellular proliferation to postpone, even to limit carcinoma growth. There was better effect in MMC group than that in control group （P 〈 0. 05）. Conclusions VEGFsiRNA and sKDR could inhibit angiogenesis and induce apoptosis in bladder carcinoma by suppressing actively bioactivity of VEGF through double pathways, being strengthened by adding MMC. The combination of anti-VEGF/KDR gene targets therapy and chemotherapy might be a therapeutic regimen of bladder carcinoma for its temptation perspective and great potential.

关 键 词：膀胱肿瘤 受体 血管内皮生长因子 丝裂霉素C 

分 类 号：R373.14[医药卫生—病原生物学]