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慢病毒介导的CD/TK融合基因转染神经干细胞治疗C6胶质母细胞瘤

Lentivirus-mediated CD/TK fusion gene transfection neural stem cell therapy for C6 glioblastoma.

作者信息

Niu Jian, Xing Chunyang, Yan Chao, Liu Hao, Cui Yuqiong, Peng Haisheng, Chen Yingli, Li Dianjun, Jiang Chuanlu, Li Nannan, Yang Haicheng

机构信息

Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, No. 148 Health Road, Nangang District, Harbin, Heilongjiang, 150000, China.

出版信息

Tumour Biol. 2013 Dec;34(6):3731-41. doi: 10.1007/s13277-013-0957-y. Epub 2013 Jul 5.

Abstract

A suicide gene can convert nontoxic prodrugs into toxic products to kill tumor cells. In this study, our aim was to transfect lentivirus-mediated CD/TK fusion gene into Wistar rat's neural stem cells (NSC) and then implant the NSC into a C6 glioma model to observe a C6 glioma growth inhibition effect. Primary NSC and stable transfection CD/TK fusion gene cell lines were established. To observe the tumor size and rat survival period in different groups, C6 glioma cell apoptosis and cell viability rate were applied to analyze the tumor inhibition effect of the neural stem cells' transfected CD/TK fusion gene. C6 cell viability showed that CDglyTK-NSC + GCV/5-Fc (group 1) was lower than CDglyTK-NSC (group 2), NSC + GCV/5-Fc (group 3), and control (group 4) from day 2 (p < 0.05), and the apoptosis rate was higher in group 1 compared with that of other groups (50.6%, p < 0.05) either in vitro or in vivo (35.47%, p < 0.05); both cell viability and apoptosis had no significance in the other three groups. In vivo, tumor size in group 1 was 7.76 ± 1.37 mm(3), which is smaller than the others (group2 27.28 ± 4.11 mm(3), group3 27.94 ± 2.08 and 28.61 ± 2.97 mm(3); p < 0.05). The other groups' tumor size was not significant (p > 0.05). Survival time of rats treated with CDglyTK-NSC + GCV/5-Fc (group 1) was significantly longer than that of the other groups (p < 0.05; group 1 48.86 ± 1.97, group 2 28.67 ± 3.75, group 3 31.5 ± 1.27, group 4 29.3 ± 1.33). We also showed that the transfected C6 cells had a migratory capacity toward gliomas in vivo. Transfected CD/TK fusion gene neural stem cells combined with propyl-guanosine and 5-flucytosine double prodrug significantly inhibit the development of glioma.

摘要

自杀基因可将无毒前体药物转化为有毒产物以杀死肿瘤细胞。在本研究中,我们的目的是将慢病毒介导的CD/TK融合基因转染到Wistar大鼠神经干细胞(NSC)中,然后将NSC植入C6胶质瘤模型中,以观察C6胶质瘤的生长抑制效果。建立了原代NSC和稳定转染CD/TK融合基因的细胞系。为观察不同组的肿瘤大小和大鼠生存期,应用C6胶质瘤细胞凋亡和细胞活力率分析转染CD/TK融合基因的神经干细胞对肿瘤的抑制作用。C6细胞活力显示,从第2天起,CDglyTK-NSC + GCV/5-Fc组(第1组)低于CDglyTK-NSC组(第2组)、NSC + GCV/5-Fc组(第3组)和对照组(第4组)(p<0.05),且第1组的凋亡率在体外和体内均高于其他组(体外50.6%,p<0.05;体内35.47%,p<0.05);其他三组的细胞活力和凋亡均无显著差异。在体内,第1组的肿瘤大小为7.76±1.37mm³,小于其他组(第2组27.28±4.11mm³,第3组27.94±2.08和28.61±2.97mm³;p<0.05)。其他组的肿瘤大小无显著差异(p>0.05)。用CDglyTK-NSC + GCV/5-Fc治疗的大鼠(第1组)的存活时间明显长于其他组(p<0.05;第1组48.86±1.97,第2组28.67±3.75,第3组31.5±1.27,第4组29.3±1.33)。我们还表明,转染的C6细胞在体内对胶质瘤具有迁移能力。转染CD/TK融合基因的神经干细胞与丙基鸟苷和5-氟胞嘧啶双前体药物联合使用可显著抑制胶质瘤的发展。

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