摘要
目的:探讨血管内皮生长因子(vascu-larendothelialgrowthfactor,VEGF)对白血病细胞生物学特性的影响。方法:台盼蓝拒染实验观察VEGF对白血病细胞增殖的影响,流式细胞术检测VEGF对化疗药物阿糖胞苷(Ara-C)所诱导的白血病细胞凋亡和胞内抗凋亡蛋白bcl-2表达的影响,用集落形成方法观察VEGF对白血病祖细胞增殖的影响。结果:50ng/mLVEGF作用白血病细胞24h,活细胞数为(3·63±1·27)×106mL-1,与阴性对照(3·23±1·60)×106mL-1差异无统计学意义。VEGF可以抵抗Ara-C200ng/mL诱导白血病细胞的凋亡。白血病细胞胞内bcl-2蛋白的阳性表达(70·78±13·36)%明显高于正常对照组(18·55±9·24)%,P=0·039。VEGF可显著延缓细胞内bcl-2表达。VEGF组:(50·85±30·46)%,阴性对照:(36·52±12·38)%。VEGF促进非红系(白血病)集落的形成。VEGF组:(49·9±29·2)/0·5mL,阴性对照:(36·5±12·4)/0·5mL,P=0·013;VEGF对红系和混合集落形成无明显影响。结论:VEGF能抵抗化疗药物Ara-C所致的白血病细胞凋亡,并促进白血病细胞集落的形成,以VEGF为AML治疗靶点可望改善患者的预后。
OBJECTIVE：To investigate the effect of vascular endothelial growth factor （VEGF） on acute myeloid leukemic cells. METHODS： Cell proliferation was detected by the trypan blue exclusion assay, the apoptosis and concentration of intracellular bcl-2 protein by flow cytometry, and the number of cells colonies by the colony-forming assay. RESULTS： The living cells number in VEGF group, which was （3.63± 1.27） × 10^6 mL^-1 was not significantly different from the negative controls （3.23±1.60）× 10^6 mL^-1. The protein level of intracellular bcl-2 in leukaemic cells group （ 70.78± 13.36） % was muchs higher than that in the normal controls （18. 55± 9.24） %, P= 0. 039; so was the intracellular bcl-2-incubation with VEGF （50.85 ± 30.46）% compared with the controls （36.52± 12.38）%. The percentage of apoptotic cells induced by Ara-C was much more than that in leukemic cells incubated with VEGF group. The number of non-erythroid colonies （49.9±29.2）/0.5 mL, with VEGF was much more than that of the control （36.5±12.4）/0.5 mL, P=0.013. VEGF did not up regulate the number of mix-colonies, but VEGF promoted the proliferation of AML stem/progenitor ceils. CONCLUSIONS： VEGF can resist leukemic cell apoptosis induced by Ara-C and promote leukemic stem/progenitor ceils. Therefore, VEGF, as a novel thoraperatic target, can improve therapy outcome in AML.
出处
《中华肿瘤防治杂志》
CAS
2006年第14期1089-1091,1094,共4页
Chinese Journal of Cancer Prevention and Treatment
