拓扑替康抑制HL-60细胞增生和诱导凋亡机制与c—myc的关系  

Inhibitory cells proliferation and induce cells apoptosis by TPT on HL-60 cell by c-myc

作　　者：王芳[1] 孙玲[1] 孙慧[1] 乐小平[2] 赵小强 

机构地区：[1]郑州大学第一附属医院血液科,450052 [2]郑州大学基础医学院组胚教研室 [3]洛阳市第三人民医院血液科

出　　处：《白血病．淋巴瘤》2008年第3期172-174,共3页Journal of Leukemia & Lymphoma

摘　　要：目的探讨拓扑替康（TPT）抑制白血病细胞的作用机制。方法采用反转录-聚合酶链反应（RT-PCR）和免疫组织化学方法，检测TPT作用后c—myc mRNA及其蛋白的表达情况。结果0．15μmol／L TPT作用HL-60细胞12h后，HL-60细胞c—myc mRNA表达为0．17±0．03，与空白对照组的1．11±0．25相比明显降低，差异具有统计学意义（P〈0．05）。HL-60细胞c—myc蛋白表达阳性细胞百分率为19．67％，较空白对照组的68．33％明显降低，差异具有统计学意义（P〈0．05）。结论拓扑替康抑制HL-60细胞增生和诱导凋亡可能是通过c—myc途径起作用的。Objective The effects of TPT on the induction of apoptosis of leukemia cells and the regulation of c-myc in mRNA and protein level. Methods RT-PCR method was adopted to examine the expressions of the genes and immuno histochemistry for the proteins of c-myc in HL-60 cells treated with TPT of optimal concentration and time. Results After HL-60 cells by TPT of 0.15 μmol/L for 12 h, the expression of c-myc mRNA decreased markedly assayed by RT-PCR. There was a significant difference between the TPT group and the control group（0.17±0.03 vs 1.11±0.25, P 〈0.05）, expressive c-myc protein decreased assayed by evidently immunoh^stochemistry. The percentage of positive cells expressing c-myc protein was a significant difference between the TPT treated group and the control group （19.67 % vs 68.33 %, P 〈0.05）. Conclusion TPT down-regulates endogenic c-myc mRNA and c-myc protein in HL-60 cells.

关 键 词：HL-60细胞 原癌基因蛋白质c—myc 拓扑替康 

分 类 号：R733[医药卫生—肿瘤]