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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。
Objective To study the effect of Ara-C on the expression of costimulatory molecules in drug-resistant leukemia cells and to explore its molecular mechanism. Methods The expressions of CD80 and CD86 on K562 and K562 / A02 cells treated with Ara-C were detected by flow cytometry. The expressions of CD80 and CD86 mRNA and the expressions of NF-κB and IAP genes were detected by RT-PCR. Results After Ara-C treatment, the expressions of CD80 and CD86 in K562 and K562 / A02 cells were significantly higher than those in control group, and downregulated the expression of NF-κB, Survivin and XIAP (X-linked inhibitor of apoptosis) , CIAP2 (cellular inhibitor of apoptosis-1,2) gene expression did not change significantly. Conclusions Ara-C can up-regulate costimulatory molecules CD80 and CD86 of drug-resistant leukemia cells and related gene NF-κB. The IAP family is an important gene participating in the up-regulation of CD80 and CD86 molecules.