地西他滨对造血系统肿瘤细胞热休克蛋白22表达的影响

Effects of decitabine on heat-shock protein 22 expression in malignant hematopoietic cells

目的探讨地西他滨（Aza-C）对造血系统肿瘤细胞热休克蛋白22（HSP22）表达的影响及可能的机制。方法半定量反转录聚合酶链反应（PCR）法检测HSP22在造血系统肿瘤细胞系以及造血系统肿瘤患者骨髓单个核细胞中的表达水平；去甲基化药物Aza—C（2μmol／L）诱导上述细胞HSP22的表达；甲基化特异PCR法检测造血系统肿瘤细胞系、造血系统肿瘤患者和健康供者的骨髓单个核细胞中HSP22基因启动子甲基化状态。结果在检测的13个造血系统肿瘤细胞系、20例不同类型的造血系统肿瘤患者以及10名健康供者骨髓单个核细胞中均未发现HSP22基因的表达；Aza-C能诱导造血系统肿瘤细胞系及造血系统肿瘤患者骨髓单个核细胞中的HSP22表达；Aza-C处理过的造血系统肿瘤细胞系中HSP22基因启动子处于部分去甲基化状态，健康供者及造血系统肿瘤患者骨髓单个核细胞HSP22基因启动子处于高甲基化状态。结论Aza—C通过使HSP22基因启动子去甲基化诱导造血系统肿瘤细胞HSP22的表达。

Objective To investigate the effects and possible mechanisms of decitabine on heat-shock protein 22 （I-ISP22） expression in hematopoietic tumor cell lines and bone marrow samples from patients with hematopoietic tumor. Methods The expression of HSP22 in 13 hematopoietic tumor cell lines, 20 primary patients＂ samples and 10 normal donor＂ samples were detected by semi-quantitative reverse transcription polymerase chain reaction （RT-PCR）. After HSP22 induction with a demethylating agent decitabine （2 I.~mol/ L）, the methylation of the HSP22 promoters in hematopoietic tumor cell lines, healthy donors and bone marrow samples from patients with hematopoietic tumor were detected by methylation specific PCR （MSP）. Results Expression of HSP22 was not detected in I3 hematopoietic tumor cell lines, 20 primary patients＂ samples or 10 healthy donors＂ samples. Decitabine can induce the expression of HSP22 in hematopoietic tumor cell lines and bone marrow samples from patients with hematopoietic tumor. Decitabine can maintain partially demethylation of HSP22 promoters in hematopoietic tumor cell lines. HSP22 promoters were highly methylated in BMMC of the healthy donors and patients with hematopoietic tumor. Conclusion Decitabine can induce the expression of HSP22 in hematopoietic tumor cells partly by demethylation of HSP22 promoters.