Yang Zijiang, Gong Weiyi, Zhang Ting, Gao Heng
Department of Neurosurgery, Affiliated Kunshan Hospital of Jiangsu University, Kunshan, China.
Department of Central Laboratory, Jiangyin Clinical College of Xuzhou Medical College, Jiangyin, China.
Front Oncol. 2021 Sep 30;11:729137. doi: 10.3389/fonc.2021.729137. eCollection 2021.
Gliomas are among the most common intracranial tumors which originated from neuroepithelial cells. Increasing evidence has revealed that long noncoding RNA (lncRNA)-microRNA (miRNA)-mRNA module regulation and tumor-infiltrating immune cells play important regulatory roles in the occurrence and progression of gliomas. However, the precise underlying molecular mechanisms remain largely unknown. Data on gliomas in The Cancer Genome Atlas lack normal control samples; to overcome this limitation, we combined 665 The Cancer Genome Atlas glioma RNA sequence datasets with 188 Genotype-Tissue Expression normal brain RNA sequences to construct an expression matrix profile after normalization. We systematically analyzed the expression of mRNAs, lncRNAs, and miRNAs between gliomas and normal brain tissues. Kaplan-Meier survival analyses were conducted to screen differentially expressed mRNAs, lncRNAs, and miRNAs. A prognostic miRNA-related competitive endogenous RNA network was constructed, and the core subnetworks were filtered using 6 miRNAs, 3 lncRNAs, and 11 mRNAs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed to investigate the biological functions of significantly dysregulated mRNAs. Co-expression network analysis was performed to analyze and screen the core genes. Furthermore, single-sample Gene Set Enrichment Analysis and immune checkpoint gene expression analysis were performed, as co-expression analysis indicated immune gene dysregulation in glioma. Finally, the expression of representative dysregulated genes was validated in U87 cells at the transcriptional level, establishing a foundation for further research. We identified 7017 mRNAs, 437 lncRNAs, and 9 miRNAs that were differentially expressed in gliomas. Kaplan-Meier survival analysis revealed 5684 mRNAs, 61 lncRNAs, and 7 miRNAs with potential as prognostic signatures in patients with glioma. The hub subnetwork of the competing endogenous RNA network between PART1-hsa-mir-25-SLC12A5/TACC2/BSN/TLN2/ZDHHC8 was screened out. Gene co-expression network, single-sample Gene Set Enrichment Analysis, and immune checkpoint expression analysis demonstrated that tumor-infiltrating immune cells are closely related to gliomas. We identified novel potential biomarkers to predict survival and therapeutic targets for patients with gliomas based on a large-scale sample. Importantly, we filtered pivotal genes that provide valuable information for further exploration of the molecular mechanisms underlying glioma tumorigenesis and progression.
胶质瘤是起源于神经上皮细胞的最常见颅内肿瘤之一。越来越多的证据表明,长链非编码RNA(lncRNA)-微小RNA(miRNA)-信使RNA(mRNA)模块调控以及肿瘤浸润免疫细胞在胶质瘤的发生和发展中发挥着重要的调控作用。然而,其确切的潜在分子机制仍 largely 未知。癌症基因组图谱中关于胶质瘤的数据缺乏正常对照样本;为克服这一局限性,我们将 665 个癌症基因组图谱胶质瘤 RNA 序列数据集与 188 个基因型-组织表达正常脑 RNA 序列相结合,在标准化后构建表达矩阵概况。我们系统地分析了胶质瘤与正常脑组织之间 mRNA、lncRNA 和 miRNA 的表达情况。进行 Kaplan-Meier 生存分析以筛选差异表达的 mRNA、lncRNA 和 miRNA。构建了一个与预后相关的 miRNA 竞争性内源 RNA 网络,并使用 6 个 miRNA、3 个 lncRNA 和 11 个 mRNA 对核心子网进行了筛选。进行基因本体论和京都基因与基因组百科全书富集分析以研究显著失调的 mRNA 的生物学功能。进行共表达网络分析以分析和筛选核心基因。此外,由于共表达分析表明胶质瘤中免疫基因失调,因此进行了单样本基因集富集分析和免疫检查点基因表达分析。最后,在 U87 细胞中对代表性失调基因的表达进行了转录水平验证,为进一步研究奠定了基础。我们鉴定出 7017 个在胶质瘤中差异表达的 mRNA、437 个 lncRNA 和 9 个 miRNA。Kaplan-Meier 生存分析揭示了 5684 个 mRNA、61 个 lncRNA 和 7 个 miRNA 具有作为胶质瘤患者预后标志物的潜力。筛选出了 PART1-hsa-mir-25-SLC12A5/TACC2/BSN/TLN2/ZDHHC8 之间竞争性内源 RNA 网络的核心子网。基因共表达网络、单样本基因集富集分析和免疫检查点表达分析表明肿瘤浸润免疫细胞与胶质瘤密切相关。我们基于大规模样本鉴定出了预测胶质瘤患者生存和治疗靶点的新型潜在生物标志物。重要的是,我们筛选出了关键基因,为进一步探索胶质瘤发生和发展的分子机制提供了有价值的信息。