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阿糖胞苷上调耐药白血病细胞共刺激分子表达及其分子机制研究
Up-regulation of costimulatory molecules by cytarabine(Ara-C)in leukemia cells and its molecular mechanism
【摘要】 目的研究阿糖胞苷(Ara-C)对耐药白血病细胞共刺激分子表达的影响,并探讨其分子机制。方法以流式细胞术检测K562和K562/A02细胞经Ara-C处理后CD80、CD86分子的表达,进而用RT-PCR方法检测CD80、CD86 mRNA表达以及NF-κB、IAP家族基因表达。结果经Ara-C处理后,K562和K562/A02细胞的CD80、CD86分子表达较对照组明显升高,并且能够下调NF-κB、Survivin、XIAP(X-linked inhibitor of apoptosis)基因表达,而cIAP1、cIAP2(cellular inhibitor of apoptosis-1,2)基因表达变化不明显。结论Ara-C可上调耐药白血病细胞共刺激分子CD80、CD86,相关基因NF-κB、IAP家族为参与其上调CD80和CD86分子的重要基因。
【Abstract】 Objective To explore the effect and mechanism of cytarabine(Ara-C)on the expression of costimulatory molecules in leukemia cells.Methods The expression of CD80 and CD86 was examined on the sur- face of K562 and K562/A02 cells by flow cytometric analysis after treatment by Ara-C CD80 and CD86 mRNA in Ara-C treated K562 and K562/A02 cells were detected by reverse transcription-PCR(RT-PCR).Results Up-reg- ulation of CD80 and CD86 at various levels was observed with leukemia cells treated by Ara-C.Ara-C induced higher expression of CD80 and CD86 mRNA on K562 and K562/A02 cells,down-regulated NF-κB,Survivin,XI- AP expression in K562 and K562/A02 cells.Conclusion Ara-C improves the expression of CD80 and CD86 in leukemia cells.NF-κB,IAP are important transcription factors involved in the up-regulation of CD80,CD86.
- 【文献出处】 中华微生物学和免疫学杂志 ,Chinese Journal of Microbiology and Immunology , 编辑部邮箱 ,2007年09期
- 【分类号】R96;R733.7
- 【被引频次】4
- 【下载频次】59