The identification of key biomarkers in patients with lung adenocarcinoma based on bioinformatics

The identification of key biomarkers in patients with lung adenocarcinoma based on bioinformatics
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DOI:
10.3934/mbe.2019384
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发表时间:
2019-01-01
影响因子:
2.6
通讯作者:
Sun, Gaozhong
Sun, Gaozhong
中科院分区:
工程技术4区
文献类型:
--
作者:
Ni, Kewei;Sun, Gaozhong

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肺腺癌(LUAD)是全球癌症死亡的主要原因之一。本研究旨在探讨LUAD的潜在机制,并确定关键的生物标志物。从GEO数据库获得LUAD相关基因表达数据集(GSE 10072)。利用GEO 2 R工具筛选LUAD患者与正常人的差异表达基因。随后,基因本体论(GO)和京都基因和基因组百科全书(KEGG)的分析,找出这些DEG的富集途径。同时,蛋白质-蛋白质相互作用(PPI)网络也被用来构建可视化这些DEG的相互作用。最后,通过GEPIA对top5上调和下调基因进行生存分析,以了解它们对LUAD的潜在影响。在我们的研究中,共捕获了856个DEG,其中559个上调基因和297个下调基因。其中,AGER、SFTPC、FABP 4、CYP 4 B1和WIF 1基因表达上调前5位,GREM 1、SPINK 1、MMP 1、COL 11 A1和SPP 1基因表达下调前5位。GO分析表明,这些DEG主要富集在DNA合成、细胞粘附、信号转导和细胞凋亡中。KEGG分析显示,富集的信号通路包括肿瘤信号通路、PI 3 K/Akt信号通路、MAPK信号通路和细胞周期。生存分析显示ZG 16的表达水平可能与LUAD患者的预后有关。根据这些DEG的连接程度,我们筛选出了前15个HUB基因,即IL 6、MMP 9、EDN 1、FOS、CDK 1、CDH 1、BIRC 5、VWF、UBE 2C、CDKN 3、CDKN 2A、CD 34、AURKA、CCNB 2和EGR 1,这些基因有望成为LUAD治疗的靶点。本研究揭示了LUAD的潜在生物标志物和候选靶点,为LUAD的诊断和治疗提供了理论依据。
Lung adenocarcinoma (LUAD) is one of the leading causes of cancer death globally. This study aims to investigate the underlying mechanisms implicated with LUAD and identify the key biomarkers. LUAD-associated gene expression dataset (GSE10072) was obtained from GEO database. Based on the GEO2R tool, we screened the differentially expressed genes (DEGs) between the patients with LUAD and normal individuals. Subsequently, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were employed to find out the enriched pathways of these DEGs. Meanwhile, a protein-protein interaction (PPI) network was also employed to construct to visualize the interactions of these DEGs. Finally, the survival analysis of the top5 up-regulated and top5 down-regulated genes were conducted via GEPIA, aiming to figure out their potential effects on LUAD. In our study, a total of 856 DEGs were captured, including 559 up-regulated genes and 297 down-regulated genes. Among these DEGs, the top5 up-regulated genes were AGER, SFTPC, FABP4, CYP4B1 and WIF1 while the top5 down-regulated genes were GREM1, SPINK1, MMP1, COL11A1 and SPP1. GO analysis disclosed that these DEGs were mainly enriched in DNA synthesis, cell adhesion, signal transduction and cell apoptosis. KEGG analysis unveiled that the enriched pathway included pathways in cancer, PI3K/Akt signaling pathway, MAPK signaling pathway and cell cycle. Survival analysis showed that the expression level of ZG16 may correlate with the prognosis of LUAD patients. Furthermore, according to the connectivity degree of these DEGs, we selected the top15 hub genes, namely IL6, MMP9, EDN1, FOS, CDK1, CDH1, BIRC5, VWF, UBE2C, CDKN3, CDKN2A, CD34, AURKA, CCNB2 and EGR1, which were expected to be promising therapeutic target in LUAD. In conclusion, our study disclosed potential biomarkers and candidate targets in LUAD, which could be helpful to the diagnosis and treatment of LUAD.