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小干扰RNA介导的iASPP下调促进拓扑替康和柔红霉素在表达野生型p53的白血病细胞中诱导的凋亡。

siRNA-mediated down-regulation of iASPP promotes apoptosis induced by etoposide and daunorubicin in leukemia cells expressing wild-type p53.

作者信息

Liu Hang, Wang Min, Diao Shiyong, Rao Qing, Zhang Xinwei, Xing Haiyan, Wang Jianxiang

机构信息

State Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Science & Peking Union Medical College, Tianjin 300020, China.

出版信息

Leuk Res. 2009 Sep;33(9):1243-8. doi: 10.1016/j.leukres.2009.02.016. Epub 2009 Mar 18.

Abstract

Oncoprotein inhibitory member of the ASPP family (iASPP) is a key inhibitor of tumor suppressor p53. Our previous study revealed that the expression of iASPP in acute leukemia (AL) patients was higher than that of normal control which implied that iASPP might play an important role in the pathogenesis and/or disease progression of AL. In this study, the iASPP expression was blocked by RNA interference (RNAi) in two leukemic cell lines, Nalm6 and K562, to explore the effects of iASPP on leukemia cells. The results indicated that down-regulation of endogenous iASPP increased p53-dependent apoptosis of leukemia cells. Thus, iASPP could be a molecular target in leukemia therapy.

摘要

ASPP家族的癌蛋白抑制成员(iASPP)是肿瘤抑制因子p53的关键抑制剂。我们之前的研究表明,急性白血病(AL)患者中iASPP的表达高于正常对照,这意味着iASPP可能在AL的发病机制和/或疾病进展中起重要作用。在本研究中,通过RNA干扰(RNAi)阻断了两种白血病细胞系Nalm6和K562中iASPP的表达,以探讨iASPP对白血病细胞的影响。结果表明,内源性iASPP的下调增加了白血病细胞中p53依赖性凋亡。因此,iASPP可能是白血病治疗的分子靶点。

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