Gene expression analysis of 12 B-cell Chronic Lymphocytic Leukemia samples and 5 CD19+ control samples. Homo sapiens
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Elevated levels of microRNA miR-155 represent a candidate pathogenic factor in chronic B-lymphocytic leukemia (B-CLL). In this study, we present evidence that MYB (v-myb myeloblastosis viral oncogene homolog) is overexpressed in a subset of B-CLL patients. MYB physically associates with the promoter of MIR155 host gene (MIR155HG, also known as BIC, B-cell integration cluster) and stimulates its transcription. This coincides with the hypermethylated histone H3K4 residue and spread hyperacetylation of H3K9 at MIR155HG promoter. Our data provide evidence of oncogenic activities of MYB in B-CLL that include its stimulatory role in MIR155HG transcription. We have studied differentially expressed genes in the whole genome and also in the preselected groups of MYB target genes and miR-155 microRNA predicted targets. Overall design: This study was intended to investigate differentially expressed genes mRNA in 12 B-CLL patient peripheral blood samples in comparison with 5 CD19+ healthy donor peripheral blood samples.
微小RNA(microRNA)miR-155的高表达,是慢性B淋巴细胞白血病(chronic B-lymphocytic leukemia, B-CLL)的潜在致病因素。本研究中,我们证实MYB基因(v-myb成髓细胞瘤病毒癌基因同源物,v-myb myeloblastosis viral oncogene homolog)在部分B-CLL患者中呈高表达状态。MYB可与MIR155宿主基因(MIR155HG,亦称BIC,即B细胞整合簇(B-cell integration cluster))的启动子区域特异性结合,并激活其转录。这一现象与MIR155HG启动子区域的组蛋白H3K4高甲基化以及H3K9广泛高乙酰化状态相一致。本研究数据证实了MYB在B-CLL中的致癌活性,其中包括其对MIR155HG转录的激活作用。我们对全基因组差异表达基因,以及预先筛选得到的MYB靶基因集和miR-155预测靶基因集进行了分析。实验整体设计:本研究旨在对比12例B-CLL患者外周血样本与5例CD19阳性健康供者外周血样本中的mRNA差异表达基因。




