高通量测序和微阵列数据分析鉴定胶质母细胞瘤中微核糖核酸的关键特征

A. Pushkin, E. A. Dzenkova, Natalya N. Timoshkina, D. Gvaldin
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引用次数: 1

摘要

研究目的:本研究旨在利用癌症基因组图谱(TCGA)数据研究胶质母细胞瘤中mRNA和miRNA的表达模式,寻找决定患者生存预后的遗传决定因素,并建立胶质母细胞瘤的相互作用网络。材料和方法。基于开放的TCGA数据库数据,形成胶质母细胞瘤和常规正常脑组织样本组。提取每个样本的存活基因和miRNA表达数据。数据分组分层后进行差异表达分析,寻找影响患者生存的基因。通过功能隶属关系和相互作用组分析进行了富集分析。共有156个胶质母细胞瘤样本具有mRNA测序数据,571个样本具有微阵列microRNA分析数据,15个对照样本进行分析。建立了mRNA-miRNA相互作用的网络,并开发了胶质母细胞瘤特征的基因和mirna的表达谱。我们确定了异常水平与生存相关的基因,并显示了microRNA的DEG和DE的两两相关。胶质母细胞瘤的microRNA-mRNA调控对可以刺激基于肿瘤发生的亚型特异性调控机制的新治疗方法的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Data analysis of high-throughput sequencing and microarray to identify key signatures of microribonucleic acids in glioblastoma
Purpose of the study. This research was devoted to study of mRNA and miRNA expression patterns in glioglastomas using The Cancer Genome Atlas (TCGA) data, to search for genetic determinants that determine the prognosis of patient survival and to create of interaction networks for glioblastomas.Materials and methods. Based on the data of the open TCGA database groups of glioblastomas and conventionally normal brain tissue samples were formed. Survival gene and miRNA expression data were extracted for each sample. After the data stratification by groups the differential expression analysis and search the genes affecting patient survival was carried out. The enrichment analysis by functional affiliation and an interactome analysis were performed.Results. A total of 156 glioblastoma samples with mRNA sequencing data, 571 samples with microarray microRNA analysis data, and 15 control samples were analyzed. Networks of mRNA-miRNA interactions were built and expression profiles of genes and miRNAs characteristic of glioblastomas were developed. We have determined the genes which aberrant level is associated with survival and shown the pairwise DEG and DE of microRNA correlations.Conclusion. The microRNA-mRNA regulatory pairs identified for glioblastomas can stimulate the development of new therapeutic approaches based on subtype-specific regulatory mechanisms of oncogenesis.
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