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Hsp701A的RNA干涉诱导K562细胞凋亡
引用本文:朱青,张王刚,王立锋,王芳,张勇,杨安钢. Hsp701A的RNA干涉诱导K562细胞凋亡[J]. 细胞与分子免疫学杂志, 2006, 22(4): 480-482,484
作者姓名:朱青  张王刚  王立锋  王芳  张勇  杨安钢
作者单位:1. 西安交通大学医学院,第一附属医院肿瘤中心,陕西,西安,710061
2. 西安交通大学医学院,第二附属医院血液内科,陕西,西安,710004
3. 第四军医大学免疫学教研室,陕西,西安,710032
基金项目:国家高技术研究发展计划(863计划)
摘    要:目的:研究RNA干涉(RNAi)Hsp701A基因的表达及其诱导慢性粒细胞白血病(慢粒)细胞株K562的凋亡。方法:构建Hsp701A基因小干涉RNA(siRNA)的真核表达载体,转染K562细胞并证实RNAi的有效性。用MTF比色法、AnnexinV-FITC/PI染色和流式细胞术,分别检测K562细胞的增殖、凋亡和细胞周期。结果:构建了Hsp701A siRNA的真核表达载体。将其稳定转染K562细胞后,RNAi组细胞中Hsp701 ARNA和蛋白的表达水平明显下降。Hsp701A siRNA能抑制K562细胞增殖并诱导其细胞凋亡,将其阻滞于G1期。结论:RNAi Hsp701A基因诱导的表达有望成为一种新的慢粒的治疗策略。

关 键 词:RNA干涉  热休克蛋白70  慢性粒细胞白血病  细胞凋亡
文章编号:1007-8738(2006)04-0480-04
收稿时间:2006-04-12
修稿时间:2006-04-122006-04-29

Knockdown of Hsp701A induces K562 cells apoptosis by RNA interference
ZHU Qing,ZHANG Wang-gang,WANG Li-feng,WANG Fang,ZHANG Yong,YANG An-gang. Knockdown of Hsp701A induces K562 cells apoptosis by RNA interference[J]. Chinese journal of cellular and molecular immunology, 2006, 22(4): 480-482,484
Authors:ZHU Qing  ZHANG Wang-gang  WANG Li-feng  WANG Fang  ZHANG Yong  YANG An-gang
Affiliation:Department of Medical Oncology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China. araa@sohu.com
Abstract:AIM: To investigate the apoptosis of K562 cells induced by RNA interference(RNAi) targeting Hsp701A. METHODS: Small interference RNA (siRNA) targeting Hsp701A was generated and its eukaryotic expression vectors was constructed and transected into K562 cells. Proliferation, apoptosis and cell cycle of the transected cells was respectively detected by MTT colorimetry and FCM. RESULTS: The eukaryotic expression vector of siRNA against Hsp701A was successfully constructed and transfected into K562 cells, which markedly decreased the expression of Hsp701A on both mRNA and protein level. K562 cells transfected with the vector exhibited slower proliferation, increased apoptosis and increased G_0/G_1 arrest. CONCLUSION: The inhibition of Hsp701A gene by RNAi may provide a foundation for the development of novel therapeutic strategy for chronic granulocyte leukemia (CML).
Keywords:RNA interference  heat shock protein 70  chronic granulocyte leukemia (CML)  apoptosis
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