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机构地区:[1]安徽省蚌埠医学院第一附属医院血液科,233000
出 处:《白血病.淋巴瘤》2012年第10期607-610,共4页Journal of Leukemia & Lymphoma
基 金:安徽省卫生厅基金(20088002)
摘 要: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10[(PRDM101)表达的影响。方法四甲基偶氮唑蓝(MTr)法检测5-Aza.CdR对NAMALWA细胞株增殖的影响,SYBRGreen相对定量反转录聚合酶链反应方法检测PRDM10α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,△Cf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。Objective To explore the effect of DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-Aza-CdR) on proliferation and tumor suppressor gene PRDMlet expression in Burkitt' s lymphoma cell line NAMALWA. Methods MTF 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-Aza- CdR 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-expressi0n of PRDM1α, and ACt 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 NAMALWA, and the possible mechanism of this inhibition may be induction of demethylation and re-expression of PRDMlet.
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