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机构地区:[1]第三军医大学新桥医院全军肿瘤诊治研究所,重庆400037
出 处:《第三军医大学学报》2008年第9期791-794,共4页Journal of Third Military Medical University
基 金:国家自然科学基金(30772144)~~
摘 要:目的探讨Bmi-1 siRNA对人白血病K562细胞增殖的影响及其作用机制。方法通过脂质体将化学合成针对Bmi-1基因的siRNA转染K562细胞,采用MTT法观察Bmi-1 siRNA对K562细胞增殖的抑制作用;流式细胞术分析细胞周期变化;Western blot检测Bmi-1siRNA对K562细胞中Bmi-1和P16蛋白表达的影响。结果Bmi-1 siRNA能明显延长K562细胞的倍增时间、G1期比例增加;下调Bmi-1表达的同时上调P16蛋白表达。结论体外化学合成的Bmi-1 siRNA对K562细胞的体外增殖具有明显的抑制作用,下调Bmi-1蛋白表达的同时上调P16蛋白表达。Objective To explore the silence of B-cell specific Moloney murine leukaemia virus insertion site 1 ( Bmi-1 ) by RNA interference on the proliferation of human leukemia cell line K562 and its mechanisms. Methods Small interfering RNA (siRNA) targeting Bmi-1 gene was designed and double-stranded siRNA was chemically synthesized. After double-stranded siRNA was transfected into K562 cells with Lipofectamine 2000, the proliferation of K562 cells was detected by MTT colorimetry, cell cycle was determined by flow cytometry, and the expression of Bmi-1 and P16 were analyzed by Western blotting. Results The siRNA targeting human Bmi-1 gene effectively prolonged the double time of K562 cells, increased the percentage of cells at G1 phase, and the expression of Bmi-1 was significantly down-regulated but the expression of P16 was up-regulated. Conclusion The siRNA targeting human Bmi-1 gene inhibits the proliferation of K562 cells, and up-regulates the expression of P16 in the cells.
关 键 词:BMI-1基因 小分子干扰RNA 人白血病K562细胞 P16蛋白
分 类 号:R394.3[医药卫生—医学遗传学] R73-354[医药卫生—基础医学]
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