摘要
目的探讨自杀基因胞嘧啶脱氨酶(CD)和胸苷激酶(TK)在小鼠体内对K562细胞的抑制作用。方法将在慢病毒介导下已转染CDgly TK的K562细胞种植于裸鼠皮下,观察其成瘤情况和对前体药物〔环氧鸟苷(GCV)、5-氟胞嘧啶(5-FC)〕的敏感性。结果种植K562细胞和K562/CDg1y TK细胞的裸鼠分别在(7.0±1.2)和(7.1±0.9)d后长出肉眼可见的瘤块。两组裸鼠生存期分别是(52.2±5.3)和(54.2±3.7)d,差异无统计学意义(P>0.05);接种K562/CDgly TK细胞的小鼠经GCV和5-FC处理后,其裸鼠分别在(26.9±1.7)、(25.7±1.9)d后肉眼可见肿瘤生长,对照组接种K562细胞后(6.9±1.7)d生长出肉眼可见肿瘤,两者差异有统计学意义(P<0.01)。结论自杀基因在体内对K562细胞有明显的抑制作用,能增强前体药物GCV和5-FC对肿瘤细胞的药物作用。
Objective To explore the inhibitory effect of suicide genes （CD and TK） on K562 cells in mice. Methods The K562 cells transfected with CDgly TK which was mediated by lentivirus were implanted in nude mice subcutaneously. The tumorigenesis and the sensitivity to the drug precursors [ganciclovir （GCV）, 5-fluorocytosine （5-FC）] were observed according to schedule. Results The nude mice implanted with K562 cells （control group） and K562/CDgly TK cells （laboratory group） erupted macroscopic tumor at day （7.0土1.2） and （7.1土0.9） respectively. The life span of nude mice in two groups was （52.2土5.3） and （54.2土3.7） days respectively, and there was no significant difference （P〉0.05） between two groups. The mice inoculated with CDgly TK cells were treated with GCV and 5-FC, and the nude mice erupted macroscopic tumor at day （26.9-1-1.7） and （25.7 ± 1.9） respectively; the mice in control group inoculated with K562 cells erupted macroscopic tumor at day （6.9±1.7） naturally, and the difference between two groups was statistically significant （P〈0.01）. Conclusion Suicide genes in the body can exert obvious inhibitory effect on K562 cells, and enhance the drug action of GCV and 5-FC on tumor cells.
出处
《检验医学与临床》
CAS
2008年第13期790-791,共2页
Laboratory Medicine and Clinic
