Objective To explore the effect of DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-Aza-CdR) on proliferation and tumor suppressor gene PRDM1α expression in Burkitt's lymphoma cell line NAMALWA. Methods MTT was used to study the impact of DNA methylation inhibitor on proliferation in NAMALWA cells,and comparative real-time reverse transcription-polymerase chain reaction (RQ-PCR) with SYBR Green assay was used to detect PRDM1α gene expression. Results MTT results showed that 5-AzaCdR inhibited proliferation of NAMALWA cells in a dose-dependent manner.After treated with 5-Aza-CdR for 72 h at 0.01,0.0625,0.1,0.125,0.25,0.5,1,2 and 4 μmol/L,the inhibition rates were 21.93 ％,39.23 ％,47.69 ％,50.37 ％,53.54 ％,57.72 ％,62.31％,65.68 ％,67.87 ％,respectively,and the differences of absorbance among the groups were also statistically significant (all P＜ 0.01). Meanwhile, 5-Aza-CdR could induce the re-expression of PRDM1α, and △Ct of 0.5, 1, 2 μmol/L groups showed significant differences compared with control group (all P ＜ 0.05). Conclusion DNA methylation inhibitor 5-Aza-CdR can significantly inhibit the proliferation of Burkitt' s lymphoma cell line NAM ALWA,and the possible mechanism of this inhibition may be induction of demethylation and re-expression of PRDM 1α.%目的 探讨DNA甲基化抑制剂5-氮杂-2’-脱氧胞苷(5-Aza-CdR)对伯基特淋巴瘤NAMALWA细胞株增殖及抑癌基因阳性调控区锌指蛋白 1 α(PRDM1α)表达的影响.方法 四甲基偶氮唑蓝(MTT)法检测5-Aza-CdR对NAMALWA细胞株增殖的影响,SYBR Green相对定量反转录聚合酶链反应方法检测PRDM1 α基因表达水平.结果 5-Aza-CdR可抑制NAMALWA细胞的增殖,且表现为浓度依赖性,在终浓度为0.01 、0.0625、0.1 、0.125、0.25、0.5、1、2和4μmol/L时对NAMALWA细胞株的抑制率分别为21.93％、39.23％、47.69％、50.37％、53.54％、57.72％、62.31％ 、65.68％和67.87％,且不同药物浓度间吸光度值比较,差异有统计学意义(均P＜0.01).同时,5-Aza-CdR能使NAMALWA细胞株中PRDM1α重新表达,0.5、1、2μmol/L加药组与对照组比较,ACt之间差异有统计学意义(P＜0.05).结论 DNA甲基化抑制剂5-Aza-CdR能显著抑制伯基特淋巴瘤NAMALWA细胞株增殖,可能与其诱导的PRDM1α基因的去甲基化和PRDM1α的再表达有关.
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