乙型肝炎病毒引起的肝细胞癌关键生物学标志物的生物信息

StephenW

Bioinformatics Analysis of Key Biomarkers and Potential Molecular Mechanisms in Hepatocellular Carcinoma Induced by Hepatitis B Virus
Zhe Li, Jingyong Xu, Hongyuan Cui, Jinghai Song, Jian Chen, Junmin Wei

    PMID: 32443377 DOI: 10.1097/MD.0000000000020302

Abstract

Background: Hepatocellular carcinoma (HCC) accounts for up to 90% of all primary hepatic malignancies; it is the sixth most common cancer and the second most common cause of cancer mortality worldwide. Numerous studies have shown that hepatitis B virus and its products, HBV integration, and mutation can induce HCC. However, the molecular mechanisms underpinning the regulation of HCC induced by HBV remain unclear.

Methods: We downloaded 2 gene expression profiling datasets, of HBV and of HCC induced by HBV, from the gene expression omnibus (GEO) database. Differentially expressed genes (DEGs) between HCC and HBV were identified to explore any predisposing changes in gene expression associated with HCC. DEGs between HCC and adjacent healthy tissues were investigated to identify genes that may play a key role in HCC. Any overlapping genes among these DEGs were included in our bioinformatics analysis. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of overlapping genes were performed using the Metascape online database; the protein-protein interaction (PPI) network was analyzed using the STRING online database; and we obtained the hub genes of the PPI network using Cytoscape software. An overall survival (OS) analysis of hub genes was performed using km-plotter and the gene expression profiling interactive analysis (GEPIA) online database. The expression levels of hub genes were determined using the TCGA and GEPIA databases. Finally, the relationships between hub genes and tumors were analyzed using the comparative toxicogenomics database (CTD).

Results: We identified 113 overlapping genes from the 2 datasets. Using functional and pathway analyses, we found that the overlapping genes were mainly related to the AMPK signaling pathway and cellular responses to cadmium ions. C8A, SPP2, KLKB1, PROZ, C6, FETUB, MBL2, HGFAC, C8B, and ANGPTL3 were identified as hub genes and C8A, SPP2, PROZ, C6, HGFAC, and C8B were found to be significant for survival.

Conclusion: The DEGs re-analyzed between HCC and hepatitis B enable a systematic understanding of the molecular mechanisms of HCC reliant on hepatitis B virus.
Similar articles

StephenW

乙型肝炎病毒引起的肝细胞癌关键生物学标志物的生物信息学分析及潜在分子机制
李哲，徐静勇，崔宏远，宋静海，陈建，魏俊敏

    PMID：32443377 DOI：10.1097 / MD.0000000000020302

抽象

背景：肝细胞癌（HCC）占所有原发性肝恶性肿瘤的90％。它是全球第六大最常见的癌症，也是第二大最常见的癌症致死原因。大量研究表明，乙型肝炎病毒及其产物，HBV整合和突变均可诱发HCC。然而，尚不清楚支持HBV诱导的HCC调节的分子机制。

方法：我们从基因表达综合数据库（GEO）下载了2个基因表达谱数据集，分别为HBV和HBV诱导的HCC。鉴定出HCC和HBV之间的差异表达基因（DEG），以探索与HCC相关的基因表达的任何诱发性变化。研究了肝癌和邻近健康组织之间的DEG，以鉴定可能在肝癌中发挥关键作用的基因。这些DEG之间的任何重叠基因都包括在我们的生物信息学分析中。使用Metascape在线数据库对重叠的基因进行了基因本体论（GO）和《京都议定书》的基因与基因组百科全书（KEGG）分析。使用STRING在线数据库分析了蛋白质-蛋白质相互作用（PPI）网络；我们使用Cytoscape软件获得了PPI网络的中心基因。使用km-绘图仪和基因表达谱交互分析（GEPIA）在线数据库对中枢基因进行了总体生存（OS）分析。使用TCGA和GEPIA数据库确定轮毂基因的表达水平。最后，使用比较毒理基因组数据库（CTD）分析了轮毂基因与肿瘤之间的关系。

结果：我们从2个数据集中鉴定出113个重叠基因。使用功能和途径分析，我们发现重叠的基因主要与AMPK信号通路和细胞对镉离子的反应有关。 C8A，SPP2，KLKB1，PROZ，C6，FETUB，MBL2，HGFAC，C8B和ANGPTL3被鉴定为中枢基因，并且发现C8A，SPP2，PROZ，C6，HGFAC和C8B对于存活很重要。

结论：重新分析肝癌和乙肝之间的DEGs，可以系统地了解依赖于乙肝病毒的肝癌的分子机制。

StephenW

https://journals.lww.com/md-jour ... markers_and.93.aspx