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机构地区:[1]徐州医学院研究生学院2011级,江苏徐州221004 [2]徐州医学院附属医院神经外科,江苏徐州221002
出 处:《徐州医学院学报》2014年第11期794-796,共3页Acta Academiae Medicinae Xuzhou
摘 要:目的观察高迁移率族蛋白A2(HMGA2)siRNA对人脑胶质瘤细胞15251周期及增殖的影响。方法Control siRNA、HMG A2 siRNA分别转染人脑胶质瘤细胞U251,Westernblot检测HMGA2蛋白表达,流式细胞仪检测HMG A2 siRNA对人脑胶质瘤细胞U251周期的影响,细胞计数试剂盒(CCK-8)细胞增殖实验检测HMG A2 siRNA对人脑胶质瘤细胞U251增殖的影响,Westernblot实验分析HMGA2基因干涉后对人脑胶质瘤细胞U251细胞周期蛋白(Cyclin)A2、CyclinB2的影响。结果与ControlsiRNA组相比,HMGA2 siRNA组人脑胶质瘤细胞U251HMGA2蛋白表达量降低40.2%,HMGA2siRNA组人脑胶质瘤细胞U251增殖细胞数降低,并且G1期细胞数所占比例减少5.05%,G2期细胞数所占比例增加4.7%(P〈0.05),HMG A2基因干涉后人脑胶质瘤细胞U251中的Cyclin A2、Cyclin B2明显减少。结论HMGA2基因干涉后通过下调Cyclin A2、Cyclin B2蛋白的表达,使人脑胶质瘤细胞U251停滞在G2期,最终抑制了人脑胶质瘤细胞U251的增殖。Objective To observe the effect of high mobility group AT - hook 2 ( HMGA2 ) siRNA on cell cycle and proliferation of human brain glioma cells U251. Methods Control siRNA and HMGA2 siRNA were used respectively to transfect human brain glioma cells U251. The expression levels of HMGA2 in human brain glioma cells U251 were detected after HMGA2 knockdown by Western blot. The influence on the cell cycle of human brain glioma cells U251 after HMGA2 knockdown was measured by flow cytometry. The influence on the proliferation of human brain glioma cells U251 after HMGA2 knockdown was measured by using cell counting kit - 8 ( CCK - 8 ) assay. The expression levels of cyclin A2 and cyclin B2 were detected by Western blot after HMGA2 interference in human brain glioma cells U251. Results Compared with the control siRNA group, the expression of HMGA2 in the HMGA2 siRNA group decreased by 40.2% in human brain glioma cells U251. HMGA2 knockdown could drastically decrease the ability of proliferation in human brain glioma cells U251. The G2 phase ratio of cell cycle increased by 4.7% and the G1 phase ratio of cell cycle decreased by 5.05% (both P 〈0.05 ). The expression levels of cyclin A2 and cyclin B2 proteins were drastically decreased in human brain glioma cells U251 after HMGA2 interference. Conclusions Silence of HMGA2 can suppress cell growth through down - regulation of cyclin A2 and cyclin B2 proteins and make cell cycle arrest at G2/M phase.
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