摘要
目的探讨mi R-96在急性髓系白血病中的表达及调控机制。方法采用逆转录-聚合酶链反应检测mi R-96在急性髓系白血病和健康人中的表达。应用mi R-96小分子类似物转染人急性髓系白血病细胞系HL-60和K562细胞,采用CCK-8试剂盒检测mi R-96和加入阿霉素后对细胞增殖和活力影响。通过流式细胞仪检测细胞的凋亡情况。利用生物信息软件预测mi R-96的潜在靶基因,RT-PCR和WB检测靶基因m RNA和蛋白表达。结果 mi R-96在急性髓系白血病中表达降低,抑制HL-60和K562细胞增殖,促进细胞凋亡;Western blot检测显示,mi R-96显著抑制内源性KRAS的表达(P<0.05)。结论 mi R-96通过靶向KRAS基因调控急性髓系白血病细胞增殖,为急性髓系白血病治疗提供新的治疗策略。
Objective To investigate the expression and regulation mechanism of mi R-96 in acute myeloid leukemia. Methods The expression of mi R-96 in acute myeloid leukemia and healthy people was detected by reverse transcription polymerase chain reaction（RT-PCR）. mi R-96 small molecular analogue was used to transfection human acute myeloid leukemia cell line HL-60 and K562 cells. The effects of mi R-96 and adriamycin on cell proliferation and viability were detected by CCK-8 kit. The apoptosis was detected by flow cytometry. The potential target genes of mi R-96 were predicted by bioinformatics software, and m RNA and protein expression of target genes were detected by RT-PCR and WB.Results The expression of mi R-96 decreased in acute myeloid leukemia, inhibited the proliferation of HL-60 and K562 cells and promoted apoptosis. Western blot analysis showed that mi R-96 significantly inhibited the expression of endogenous KRAS（P 〈0.05）. Conclusion mi R-96 regulates the proliferation of acute myeloid leukemia cells by targeting KRAS gene and provides a new therapeutic strategy for the treatment of acute myeloid leukemia.
作者
董巧凤
杨书环
刘翠红
Dong Qiaofeng;Yang Shuhuan;Liu Cuihong(Heze Municiple Hospital,Heze 274000,Shandon)
出处
《菏泽医学专科学校学报》
2018年第2期13-15,25,共4页
Journal of Heze Medical College
