Open Access

DNA hypermethylation of aurora kinase A in hepatitis C virus‑positive hepatocellular carcinoma

  • Authors:
    • Zuohong Ma
    • Yefu Liu
    • Zhiqiang Hao
    • Xiangdong Hua
    • Wenxin Li
  • View Affiliations

  • Published online on: July 11, 2019     https://doi.org/10.3892/mmr.2019.10487
  • Pages: 2519-2532
  • Copyright: © Ma et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Changes in the methylation levels of tumor suppressor genes or proto‑oncogenes are involved in the pathogenesis of hepatitis C virus (HCV) infection‑induced hepatocellular carcinoma (HCC). The aim of the present study was to identify novel aberrantly methylated differentially expressed genes by integrating mRNA expression profile (GSE19665 and GSE62232) and methylation profile (GSE60753) microarrays downloaded from the Gene Expression Omnibus database. Functional enrichment analysis of screened genes was performed using the DAVID software and BinGO database. Protein‑protein interaction (PPI) networks were constructed using the STRING database, followed by module analysis with MCODE software. The transcriptional and translational expression levels of crucial genes were confirmed using The Cancer Genome Atlas (TCGA) datasets and Human Protein Atlas database (HPA). A total of 122 downregulated/hypermethylated genes and 63 upregulated/hypomethylated genes were identified. These genes were enriched in the Gene Ontology biological processes terms of ‘inflammatory response’ [Fos proto‑oncogene, AP‑1 transcription factor subunit (FOS)] and ‘cell cycle process’ [aurora kinase A (AURKA), cyclin dependent kinase inhibitor 3 (CDKN3) and ubiquitin conjugating enzyme E2 C (UBE2C)]. PPI network and module analysis indicated that human oncogenes FOS, AURKA, CDKN3 and UBE2C may be hub genes. mRNA, protein expression and methylation levels of AURKA and FOS were validated by TCGA and HPA data. In conclusion, aberrantly methylated AURKA and FOS may be potential therapeutic targets for HCV‑positive HCC.
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September-2019
Volume 20 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Ma Z, Liu Y, Hao Z, Hua X and Li W: DNA hypermethylation of aurora kinase A in hepatitis C virus‑positive hepatocellular carcinoma. Mol Med Rep 20: 2519-2532, 2019.
APA
Ma, Z., Liu, Y., Hao, Z., Hua, X., & Li, W. (2019). DNA hypermethylation of aurora kinase A in hepatitis C virus‑positive hepatocellular carcinoma. Molecular Medicine Reports, 20, 2519-2532. https://doi.org/10.3892/mmr.2019.10487
MLA
Ma, Z., Liu, Y., Hao, Z., Hua, X., Li, W."DNA hypermethylation of aurora kinase A in hepatitis C virus‑positive hepatocellular carcinoma". Molecular Medicine Reports 20.3 (2019): 2519-2532.
Chicago
Ma, Z., Liu, Y., Hao, Z., Hua, X., Li, W."DNA hypermethylation of aurora kinase A in hepatitis C virus‑positive hepatocellular carcinoma". Molecular Medicine Reports 20, no. 3 (2019): 2519-2532. https://doi.org/10.3892/mmr.2019.10487