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首页> 外文期刊>Cancer Cell International >Up-regulation of CTD-2547G23.4 in hepatocellular carcinoma tissues and its prospective molecular regulatory mechanism: a novel qRT-PCR and bioinformatics analysis study
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Up-regulation of CTD-2547G23.4 in hepatocellular carcinoma tissues and its prospective molecular regulatory mechanism: a novel qRT-PCR and bioinformatics analysis study

机译:肝细胞癌组织中CTD-2547G23.4的上调及其潜在分子调控机制:新型qRT-PCR和生物信息学分析研究

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Dysregulated expression of long non-coding RNAs (lncRNAs) has been reported in the pathogenesis and progression of multiple cancers, including hepatocellular carcinoma (HCC). LncRNA CTD-2547G23.4 is a novel lncRNA, and its role in HCC is still unknown. Here, we aimed to clarify the expression pattern and clinical value of CTD-2547G23.4 and to investigate the prospective regulatory mechanism via bioinformatics analysis in HCC. To identify differentially expressed lncRNAs in HCC, we downloaded RNA-Seq data for HCC and adjacent non-tumour tissues via The Cancer Genome Atlas (TCGA). CTD-2547G23.4 was selected by using the R language and receiver operating characteristic curve analysis. Furthermore, we validated the differential expression of CTD-2547G23.4 via Gene Expression Omnibus (GEO), ArrayExpress, Oncomine databases and quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between the CTD-2547G23.4 level and clinic pathological parameters was also assessed. To further probe the role of CTD-2547G23.4 in HCC cell cycle, lentivirus-mediated small interfering RNA was applied to silence CTD-2547G23.4 expression in Huh-7 cell line. In addition, the related genes of CTD-2547G23.4 gathered from The Atlas of Noncoding RNAs in Cancer (TANRIC) database and Multi Experiment Matrix (MEM) were assessed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes, Protein Analysis Through Evolutionary Relationships and protein–protein interaction (PPI) networks. CTD-2547G23.4 expression was remarkably higher in 370 HCC tissue samples than that in adjacent non-tumour liver tissues (48.762?±?27.270 vs. 14.511?±?8.341, P?
机译:长期非编码RNA(lncRNA)的表达失调已被报道在包括肝细胞癌(HCC)在内的多种癌症的发病和发展过程中。 LncRNA CTD-2547G23.4是一种新型的lncRNA,其在HCC中的作用尚不清楚。在这里,我们旨在阐明CTD-2547G23.4的表达模式和临床价值,并通过生物信息学分析来研究HCC中的前瞻性调控机制。为了鉴定HCC中差异表达的lncRNA,我们通过The Cancer Genome Atlas(TCGA)下载了HCC和邻近非肿瘤组织的RNA-Seq数据。通过使用R语言和接收器工作特性曲线分析选择了CTD-2547G23.4。此外,我们通过基因表达综合(GEO),ArrayExpress,Oncomine数据库和定量实时聚合酶链反应(qRT-PCR)验证了CTD-2547G23.4的差异表达。还评估了CTD-2547G23.4水平与临床病理参数之间的关系。为了进一步探讨CTD-2547G23.4在HCC细胞周期中的作用,应用了慢病毒介导的小干扰RNA沉默Huh-7细胞株中CTD-2547G23.4的表达。此外,通过基因本体论(GO),《京都基因与基因组百科全书》,蛋白质分析对从癌症非编码RNA地图集(TANRIC)和多实验矩阵(MEM)中收集的CTD-2547G23.4相关基因进行了评估。通过进化关系和蛋白质-蛋白质相互作用(PPI)网络。 TCGA数据集中,在370例HCC组织样品中,CTD-2547G23.4的表达明显高于相邻的非肿瘤肝组织(48.762?±?27.270与14.511?±?8.341,P?<?0.001)。根据实时RT-RT评估,HCC中CTD-2547G23.4的相对表达水平始终高于相邻的非癌性组织(2.464±0.883相对于1.813±0.784,P≤0.001)。定量PCR。根据TCGA,qRT-PCR和GEO数据,摘要接收器工作特性曲线的曲线下面积为0.8720。进一步的分析表明,CTD-2547G23.4的表达水平升高与肿瘤组织学分级和血管肿瘤细胞类型有关。 CTD-2547G23.4敲低细胞中CTD-2547G23.4的表达明显下调。此外,细胞周期分析显示,Huh-7细胞系中的CTD-2547G23.4耗尽导致S期停滞。此外,通过途径分析处理了由TANRIC和MEM数据库鉴定的314个相关基因。生物信息学分析表明,CTD-2547G23.4可能通过SRC,CREBBP,ADCY8和PPARA这四个中枢基因在肝癌的进展中起关键作用。集体地,我们提出了这样的假说,即新的lncRNA CTD-2547G23.4可以作为例外的临床指标,并通过各种相关基因促进肝癌的肿瘤发生和发展。

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