中国肿瘤生物治疗杂志2013，Vol.20Issue(1)：58-62,5.DOI:10.3872/j.issn.1007-385X.2013.01.010
慢病毒介导的HO-1基因沉默对人白血病K562细胞增殖与凋亡的影响
Effect of silencing HO-1 gene expression by lentivirus on proliferation and apoptosis of human leukemia K562 cells
摘要
Abstract
Objective: To explore the effect of silencing heme oxygenase-1 (HO-1) gene expression on proliferation and apoptosis of chronic myelogenous leukemia (CML) K562 cells. Methods: The recombinant lentivirus Lv-siRNA-HO-1 targeting HO-1 gene was constructed and then was infected into K562 cells, and multipliciy of infection (MOI) was detected by fluorescence microscopy. The expression level of HO-1 protein in K562 cells was examined by Western blotting in Lv-siRNA-HO-1 infection group, Lv-Ctrl infection group and uninfection group. The proliferation and apoptosis of K562 cells was detected by CCK-8 and flow cytometry, respectively. Results: The interference expression vector PSIH1-HO-1-siRNA targeting HO-1 gene was constructed successfully, and packaged to form recombinant lentiviral vector Lv-siRNA-HO-1, which was infected into K562 cells with MOI being 6. Compared with the uninfection group, the expression of HO-1 protein in K562 cells decreased significantly after Lv-siRNA-HO-1 infection ([0. 16 ±0.02] vs [0.70 ±0.02] , P＜0.01) , and the proliferation activity of K562 cells was also decreased significantly ( [1.36 ±0. 12] vs [2.02 ±0. 17] , P＜0.01). However, the apoptotic rate of K562 cells was significantly increased ( [62.77 ±4.39]% vs [ 14. 19 ± 1. 6 ] % ,P ＜0. 01 ]. Conclusion: Silencing HO-1 gene through lentvirus can inhibit the proliferation and induce the apoptosis of human leukemia K562 cells.关键词
血红素加氧酶1(HO-1)/白血病/K562细胞/RNA干扰/增殖活性/凋亡/慢病毒Key words
heme oxygenase-1(HO-7) / leukemia/ K562 cell/ RNA interference/ proliferation/ apoptosis/ lentivirus分类
医药卫生引用本文复制引用
马微,冯玉宽,杨玉,郭艳芹,张鹏霞..慢病毒介导的HO-1基因沉默对人白血病K562细胞增殖与凋亡的影响[J].中国肿瘤生物治疗杂志,2013,20(1):58-62,5.基金项目
黑龙江省研究生创新科研项目基金资助(No.YJSCX2011-294HLJ) （No.YJSCX2011-294HLJ）
黑龙江省卫生厅科研项目资助(No.2010-484) （No.2010-484）
佳木斯大学创新自然科学研究项目资助(No.Dz2011-075). （No.Dz2011-075）
