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首页> 外文期刊>British Journal of Haematology >Gene silencing of MIR22 in acute lymphoblastic leukaemia involves histone modifications independent of promoter DNA methylation
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Gene silencing of MIR22 in acute lymphoblastic leukaemia involves histone modifications independent of promoter DNA methylation

机译：急性淋巴细胞白血病中MIR22的基因沉默涉及组蛋白修饰，独立于启动子DNA甲基化

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摘要

SummaryAberrant epigenetic regulation has recently been implicated in the downregulation of tumour suppressor microRNAs (miRNAs). Histone modification and DNA methylation can have different roles in gene silencing in cancer. To investigate whether histone modifications would contribute to the dysregulation of miRNAs in acute lymphoblastic leukaemia (ALL), the effect of a histone deacetylase inhibitor, trichostatin A (TSA), on miRNA expression profile was analysed by microarray assay in a precursor B-cell ALL cell line NALM-6. A total of 10 miRNAs were downregulated and 31 were upregulated significantly following TSA treatment. Among TSA-upregulated miRNAs, MIR22 is an extronic miRNA and resides in the second exon of the non-coding transcript MGC14376. Upregulation of MIR22 transcription was found in both NALM-6 cells and primary human ALL malignant cells treated with TSA. Whereas a CpG island was identified within the promoter element of MIR22, no promoter DNA methylation was detected in these cells. In contrast, accumulation of the repressive histone marker H3K27 trimethylation (H3K27triM) was indentified around the transcriptional start point of the gene, which was reduced by TSA treatment. Thus, accumulation of H3K27triM independent of promoter DNA methylation may be a novel epigenetic mechanism for MIR22 silencing in ALL.
机译：总结最近，表观遗传异常调控与肿瘤抑制微RNA（miRNA）的下调有关。组蛋白修饰和DNA甲基化在癌症的基因沉默中可能具有不同的作用。为了研究组蛋白修饰是否会导致急性淋巴细胞白血病（ALL）中的miRNA失调，通过微阵列分析在前体B细胞ALL中分析了组蛋白脱乙酰基酶抑制剂曲古抑菌素A（TSA）对miRNA表达谱的影响。细胞系NALM-6。在TSA处理后，总共有10个miRNA下调，有31个显着上调。在TSA上调的miRNA中，MIR22是一个外显子miRNA，位于非编码转录本MGC14376的第二个外显子中。在用TSA处理的NALM-6细胞和原代人ALL恶性细胞中均发现MIR22转录上调。尽管在MIR22的启动子元件内鉴定出CpG岛，但在这些细胞中未检测到启动子DNA甲基化。相反，在基因的转录起始点附近发现了抑制性组蛋白标记物H3K27三甲基化（H3K27triM）的积累，这种积累通过TSA处理得以降低。因此，H3K27triM的积累与启动子DNA甲基化无关，可能是ALL中MIR22沉默的新表观遗传机制。

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  • 来源
    《British Journal of Haematology》 |2010年第1期|p.69-79|共11页
  • 作者

    Xiaoqing Li; Jun Liu; Rui Zhou; Shi Huang; Shiang Huang; Xian-Ming Chen;

  • 作者单位

    Institute of Hematology, Union Hospital, Wuhan, China|Department of Medical Microbiology and Immunology, Creighton University Medical Center, Omaha, NE;

    |Institute of Hematology, Union Hospital, Wuhan, China|Department of Medical Microbiology and Immunology, Creighton University Medical Center, Omaha, NE;

    |Department of Medical Microbiology and Immunology, Creighton University Medical Center, Omaha, NE;

    Burnham Institute for Medical Research, La Jolla, CA, USA;

    Institute of Hematology, Union Hospital, Wuhan, China;

    Department of Medical Microbiology and Immunology, Creighton University Medical Center, Omaha, NE;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    microRNAs; epigenetics; microRNA-22; histone modification; DNA methylation;

    机译：microRNAs;表观遗传学;microRNA-22;组蛋白修饰;DNA甲基化;

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