Wu Min, Liu Zhaobo, Zhang Aiying, Li Ning
Department of General surgery.
Beijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, China.
Medicine (Baltimore). 2019 Feb;98(5):e14287. doi: 10.1097/MD.0000000000014287.
Hepatocellular carcinoma (HCC) is one of the most prevalent cancers worldwide. However, the precise mechanisms of the development and progression of HCC remain unclear. The present study attempted to identify and functionally analyze the differentially expressed genes between HCC and cirrhotic tissues by using comprehensive bioinformatics analyses.
The GSE63898 gene expression profile was downloaded from the Gene Expression Omnibus (GEO) and analyzed using the online tool GEO2R to identify differentially expressed genes (DEGs). Gene ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the DEGs were performed in DAVID. The STRING database was used to evaluate the interactions of DEGs and to construct a protein-protein interaction (PPI) network using Cytoscape software. Hub genes were selected using the cytoHubba plugin and were validated with the cBioPortal database.
A total of 301 DEGs were identified between HCC and cirrhotic tissues. The GO analysis results showed that these DEGs were significantly enriched in certain biological processes including negative regulation of growth and cell chemotaxis. Several significant pathways, including the p53 signaling pathway, were identified as being closely associated with these DEGs. The top 12 hub genes were screened and included TTK, NCAPG, TOP2A, CCNB1, CDK1, PRC1, RRM2, UBE2C, ZWINT, CDKN3, AURKA, and RACGAP1. The cBioPortal analysis found that alterations in hub genes could result in significantly reduced disease-free survival in HCC.
The present study identified a series of key genes and pathways that may be involved in the tumorigenicity and progression of HCC, providing a new understanding of the underlying molecular mechanisms of carcinogenesis in HCC.
肝细胞癌（HCC）是全球最常见的癌症之一。然而，HCC发生和进展的确切机制仍不清楚。本研究试图通过全面的生物信息学分析来鉴定和功能分析HCC与肝硬化组织之间差异表达的基因。
从基因表达综合数据库（GEO）下载GSE63898基因表达谱，并使用在线工具GEO2R进行分析以鉴定差异表达基因（DEG）。在DAVID中对DEG进行基因本体（GO）功能分析和京都基因与基因组百科全书（KEGG）通路富集分析。STRING数据库用于评估DEG的相互作用，并使用Cytoscape软件构建蛋白质-蛋白质相互作用（PPI）网络。使用cytoHubba插件选择枢纽基因，并通过cBioPortal数据库进行验证。
在HCC和肝硬化组织之间共鉴定出301个DEG。GO分析结果表明，这些DEG在某些生物学过程中显著富集，包括生长的负调控和细胞趋化性。包括p53信号通路在内的几个重要通路被确定与这些DEG密切相关。筛选出前12个枢纽基因，包括TTK、NCAPG、TOP2A、CCNB1、CDK1、PRC1、RRM2、UBE2C、ZWINT、CDKN3、AURKA和RACGAP1。cBioPortal分析发现，枢纽基因的改变可能导致HCC患者无病生存期显著缩短。
本研究鉴定出一系列可能参与HCC致瘤性和进展的关键基因和通路，为HCC致癌作用的潜在分子机制提供了新的认识。
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