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Analysis of regulatory networks constructed based on gene coexpression in pituitary adenoma

机译:基于基因共表达的垂体腺瘤构建的调控网络分析

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Gene coexpression patterns can reveal gene collections with functional consistency. This study systematically constructs regulatory networks for pituitary tumours by integrating gene coexpression, transcriptional and posttranscriptional regulation. Through network analysis, we elaborate the incidence mechanism of pituitary adenoma. The Pearson's correlation coefficient was utilized to calculate the level of gene coexpression. By comparing pituitary adenoma samples with normal samples, pituitary adenoma-specific gene coexpression patterns were identified. For pituitary adenoma-specific coexpressed genes, we integrated transcription factor (TF) and microRNA (miRNA) regulation to construct a complex regulatory network from the transcriptional and posttranscriptional perspectives. Network module analysis identified the synergistic regulation of genes by miRNAs and TFs in pituitary adenoma. We identified 142 pituitary adenoma-specific active genes, including 43 TFs and99 target genes of TFs. Functional enrichment of these 142 genes revealed that the occurrence of pituitary adenoma induced abnormalities in intracellular metabolism and angiogenesis process. These 142 genes were also significantly enriched in adenoma pathway. Module analysis of the systematic regulatory network found that three modules contained elements that were closely related to pituitary adenoma, such as FGF2 and SP1, as well as transcription factors and miRNAs involved in the tumourigenesis. These results show that in the occurrence of pituitary adenoma, miRNA, TF and genes interact with each other. Based on gene expression, the proposed method integrates interaction information from different levels and systematically explains the occurrence of pituitary tumours. It facilitates the tracing of the origin of the disease and can provide basis for early diagnosis of complex diseases or cancer without obvious symptoms.
机译:基因共表达模式可以揭示具有功能一致性的基因集合。这项研究通过整合基因共表达,转录和转录后调控系统地构建垂体肿瘤的调控网络。通过网络分析,我们详细阐述了垂体腺瘤的发病机制。皮尔逊相关系数用于计算基因共表达水平。通过比较垂体腺瘤样本与正常样本,可以确定垂体腺瘤特异性基因共表达模式。对于垂体腺瘤特异性共表达基因,我们从转录和转录后的角度整合了转录因子(TF)和microRNA(miRNA)调控,以构建一个复杂的调控网络。网络模块分析确定了垂体腺瘤中miRNA和TF对基因的协同调控。我们鉴定了142个垂体腺瘤特异性活性基因,包括43个TF和99个TF靶基因。这些142个基因的功能丰富表明,垂体腺瘤的发生在细胞内代谢和血管生成过程中引起异常。这142个基因在腺瘤途径中也显着富集。系统调节网络的模块分析发现,三个模块包含与垂体腺瘤密切相关的元件,例如FGF2和SP1,以及参与肿瘤发生的转录因子和miRNA。这些结果表明在垂体腺瘤的发生中,miRNA,TF和基因彼此相互作用。该方法基于基因表达,整合了不同层次的相互作用信息,系统地解释了垂体肿瘤的发生。它有助于追踪疾病的起源,并为没有明显症状的复杂疾病或癌症的早期诊断提供基础。

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