Abstract
Chronic infection with hepatitis B virus (HBV) has long been recognized as a dominant hazard factor for hepatocellular carcinoma (HCC) and accounts for at least half of HCC instances globally. However, the underlying molecular mechanism of HBV-linked HCC has not been completely elucidated. Here, three microarray datasets, totally containing 170 tumoral samples and 181 adjacent normal tissues from the liver of patients suffering from HBV-related HCC assembled from the Gene Expression Omnibus (GEO) database, were subjected to integrated analysis of differentially expressed genes (DEGs). Subsequently, the analysis of function and pathway enrichment as well as the protein-protein interaction network (PPI) was performed. The ten hub genes screened out from the PPI network were further subjected to expression profile and survival analysis. Overall, 329 DEGs (67 upregulated and 262 downregulated) were identified. Ten DEGs with the highest degree of connectivity included cyclin-dependent kinase 1 (CDK1), cyclin B1 (CCNB1), cyclin B2 (CCNB2), PDZ-binding kinase (PBK), abnormal spindle microtubule assembly (ASPM), nuclear division cycle 80 (NDC80), aurora kinase A (AURKA), targeting protein for xenopus kinesin-like protein 2 (TPX2), kinesin family member 2C (KIF2C), and centromere protein F (CENPF). Kaplan-Meier analysis unveiled that overexpression levels of KIF2C and TPX2 were relevant to both the poor overall survival and relapse-free survival. In summary, the hub genes validated in the present study may provide promising targets for the diagnosis, prognosis, and therapy of HBV-associated HCC. Additionally, our work uncovers various crucial biological components (e.g., extracellular exosome) and signaling pathways that participate in the progression of HCC induced by HBV, serving comprehensive knowledge of the mechanisms regarding HBV-related HCC.
Highlights
Based on the new statistics in 2018, hepatocellular carcinoma (HCC) has been estimated to be the seventh most prevalent cancer and the third major cause of tumor-related death worldwide [1]
The dataset search was performed by using terms (“HCC” [Description] OR “tumor” [Description] OR “hepatocellular carcinoma” [Description]) AND (“HBV” [Description] OR “hepatitis B virus” [Description])) AND “Homo sapiens” [Organism]) AND “Expression profiling by array” [DataSet Type] in the Gene Expression Omnibus (GEO) database founded by the National Center for Biotechnology Information
Kaplan-Meier analysis from our study indicated that high expression levels of targeting protein for xenopus kinesin-like protein 2 (TPX2) and kinesin family member 2C (KIF2C) were associated with both the poor overall survival and relapse-free survival, suggesting that these two core genes may serve as valuable targets for both diagnosis and prognosis of HCC patients infected with HBV
Summary
Based on the new statistics in 2018, hepatocellular carcinoma (HCC) has been estimated to be the seventh most prevalent cancer and the third major cause of tumor-related death worldwide [1]. One of the leading risk factors for HCC is hepatitis B virus (HBV). HBV has been known as a trigger of HCC even in the absence of cirrhosis. The risk of HCC is affected by heredity, infection, and nutritional and lifestyle factors in those infected with HBV [3]. The mechanisms of HBV-related HCC have been proposed to be linked with chronic inflammation and hepatocellular regeneration [4]. Effective biomarkers for the International Journal of Genomics diagnosis, prognosis, and therapy of HBV-related HCC are urgently required in order to enhance the survival rate of patients
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