Department of Pathology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Xinjiang Medical University, Urumqi, 830011, China.
Curr Med Sci. 2020 Oct;40(5):885-899. doi: 10.1007/s11596-020-2250-9. Epub 2020 Oct 29.
Peripheral T-cell lymphoma (PTCL) is a very aggressive and heterogeneous hematological malignancy and has no effective targeted therapy. The molecular pathogenesis of PTCL remains unknown. In this study, we chose the gene expression profile of GSE6338 from the Gene Expression Omnibus (GEO) database to identify hub genes and key pathways and explore possible molecular pathogenesis of PTCL by bioinformatic analysis. Differentially expressed genes (DEGs) between PTCL and normal T cells were selected using GEO2R tool. Gene ontology (GO) analysis and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis were performed using Database for Annotation, Visualization and Integrated Discovery (DAVID). Moreover, the Search Tool for the Retrieval of Interacting Genes (STRING) and Molecular Complex Detection (MCODE) were utilized to construct protein-protein interaction (PPI) network and perform module analysis of these DEGs. A total of 518 DEGs were identified, including 413 down-regulated and 105 up-regulated genes. The down-regulated genes were enriched in osteoclast differentiation, Chagas disease and mitogen-activated protein kinase (MAPK) signaling pathway. The up-regulated genes were mainly associated with extracellular matrix (ECM)-receptor interaction, focal adhesion and pertussis. Four important modules were detected from the PPI network by using MCODE software. Fifteen hub genes with a high degree of connectivity were selected. Our study identified DEGs, hub genes and pathways associated with PTCL by bioinformatic analysis. Results provide a basis for further study on the pathogenesis of PTCL.
外周 T 细胞淋巴瘤（PTCL）是一种非常侵袭性和异质性的血液恶性肿瘤，目前尚无有效的靶向治疗方法。PTCL 的分子发病机制尚不清楚。在本研究中，我们选择了基因表达综合数据库（GEO）中 GSE6338 基因表达谱，通过生物信息学分析，鉴定出与 PTCL 相关的枢纽基因和关键通路，探索其可能的分子发病机制。使用 GEO2R 工具筛选 PTCL 与正常 T 细胞之间的差异表达基因（DEGs）。使用数据库注释、可视化和综合发现（DAVID）进行基因本体论（GO）分析和京都基因与基因组百科全书（KEGG）通路分析。此外，还使用 Search Tool for the Retrieval of Interacting Genes（STRING）和 Molecular Complex Detection（MCODE）构建蛋白质-蛋白质相互作用（PPI）网络，并对这些 DEGs 进行模块分析。共鉴定出 518 个 DEGs，包括 413 个下调基因和 105 个上调基因。下调基因在破骨细胞分化、恰加斯病和丝裂原活化蛋白激酶（MAPK）信号通路中富集。上调基因主要与细胞外基质（ECM）-受体相互作用、粘着斑和百日咳有关。通过 MCODE 软件从 PPI 网络中检测到四个重要的模块。选择了 15 个具有高连接度的枢纽基因。通过生物信息学分析，我们确定了与 PTCL 相关的 DEGs、枢纽基因和通路。这些结果为进一步研究 PTCL 的发病机制提供了依据。
