摘要
目的:探讨诱导分化剂对K562细胞增殖抑制的作用与分子机制。方法:通过MTT试验和细胞形态学观察K562细胞增殖的改变和分化情况。通过流式细胞仪实验检测细胞周期改变,RT-PCR检测EVI1、TGF-β1和WT1基因表达的变化。结果:K562细胞经六亚甲基二乙酰胺(HMBA)和(或)三氧化二砷(As2O3)作用后增殖明显受到抑制,并向不同方向分化,细胞被阻滞在G1期。K562细胞的增殖抑制作用与EVI1和WT1基因表达下调,TGF-β1基因表达上调一致。EVI1/β-actin从0.9253渐降至0.1379,WT1/β-actin从0.9953降至0.1978。TGF-β1/β-actin从0.3315增至1.2452。结论:HMBA、As2O3及其联合抑制K562细胞增殖作用与EVI1和WT1基因表达下调,TGF-β1基因表达上调有关。
OBJECTIVE： To analyze the inhibitory effect and the molecular mechanism of the induction differentiation on the multiplication of K562 cell. METHODS： The multiplication and differentiation of K562 cell were observed through the MTT experiment and the cytomorphology. The flow cytometer was used to examine the cell cycle changes, and the RT-PCR was used to test EVIl, TGF-β1and WT1 gene expression changes. RUSULTS： The muhiplication of was inhibitated K562 cell was inhibitated obviously was inhibitated by HMBA or/and As2O3. The cells were hindered in the G1 stage, which was consistent to EVIl and the WT1 gene expression declines, and TGF-β1 gene expression upward. EVI1/β-actin fell deereased from 0. 925 3 to 0. 137 9, and WT1/β-actin fell from 0. 995 3 to 0. 197 8. TGF-β1/β-actin increased from 0. 331 5 to 1. 245 2. CONCLU- SION： HMBA or/and As2O3 suppresse the K562 cell multiplica tion function which is related ro EVIl and the WT1 gene expression declines and TGF-β1 gene expression upward.
出处
《中华肿瘤防治杂志》
CAS
2008年第14期1049-1053,共5页
Chinese Journal of Cancer Prevention and Treatment
基金
国家自然科学基金(30771103)
科技部中瑞政府间合作项目(AM15B
1)
山东省优秀中青年科学家基金项目(03BS033)
山东省自然科学基金重点项目(Z2004C08)
山东省自然科学基金(Y2005C39)
山东省卫生高层次人才1020工程专项经费资助
