期刊文献+

急性髓系白血病中组蛋白去甲基化酶KDM3B和JMJD1C的差异化表达 被引量:1

Differential expression of histone demethylase KDM3B and JMJD1C inacute myeloid leukemia
下载PDF
导出
摘要 目的 探讨白血病中组蛋白去甲基化酶KDM3B和JMJD1C受到的协同调控。方法 在多个急性髓系白血病细胞株中采用细胞遗传学分析KDM3B和JMJD1C的拷贝数情况。在急性髓系白血病细胞株NB4和HL-60中,应用Daminozide进行处理,观察组蛋白H3K9单甲基化和二甲基化的情况。在急性髓系白血病细胞株NB4和HL-60中,应用Daminozide、ATRA(All-trans retinoid acid)、Vtamin C进行处理,通过实时定量PCR检测去甲基化酶KDM3B和JMJD1C的表达情况。结果 KDM3B和JMJD1C在不同的急性髓细胞白血病细胞系中拷贝数呈负相关。经Daminozide药物分别对NB4和HL-60细胞进行处理后,NB4细胞和HL-60细胞组的H3K9单甲基化和二甲基化的水平呈上升趋势。使用3种药物分别进行处理后,在NB4细胞中,KDM3B的m RNA下调,JMJD1C的m RNA水平上调;与之相反,在HL-60细胞中,表现为KDM3B的m RNA上调和JMJD1C的m RNA水平下调。结论 急性髓细胞白血病中JMJD1C和KDM3B呈负相关的表达趋势。 Objective To investigate the synergistic regulation of KDM3B and JMJD1C in leukemia. Methods The expression level o f JMJD1C and KDM3B were analyzed in multiple acute myeloid leukemia (AML) cell lines. AML cell lines NB4 and HL-60 were treated with Daminozide, followed by detennination of H3K9 mono-methylation and di-methylation. AML cell lines NB4 and HL-60 were treated with Daminozide, ATRA (retinoid acid All-trans), C Vitamin and the expression of KDM3B and JMJD1C were detected by real-time quantitative PCR. Results The expression level of KDM3B and JMJD1C in the AML cell lines was negatively correlated. In NB4 and HL-60 cells treated by daminozide, H3K9 mono-methylation and di_ methylation level showed a rising trend in these two cell groups. After treatment of NB4 cells with the 3 reagents, the level of mRNA of KDM3B was down-regulated while the level of mRNA of JMJD1C was up-regulated. In HL-60 cells treated by daminozide, the tnRNA level of KDM3B was up-regulated and the mRNA level of JMJD1C was down-regulated. Conclusion The expression o f KDM3B and JMJD1C is negatively correlated in patients with AML.
出处 《中国生化药物杂志》 CAS 2017年第1期27-30,共4页 Chinese Journal of Biochemical Pharmaceutics
基金 国家自然科学基金(81570157,81370628) 教育部海外归国学者科学研究基金(81570157) 山东省医药卫生科技发展计划项目(2013WSB28012)
关键词 急性髓系白血病 组蛋白修饰酶 KDM3B JMJD1C acute myeloid leukemia histx)ne modifying enzymes KDM3B JMJDlC
  • 相关文献

同被引文献15

引证文献1

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部