Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death. The aim of this study was to identify underlying hub genes and dysregulated pathways associated with the development of HCC using bioinformatics analysis. Differentially expressed protein-coding genes were subjected to transcriptome sequencing in 11 pairs of liver cancer tissue and matched adjacent non-cancerous tissue. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed, followed by protein-protein interaction (PPI) network construction. Hub genes were identified via centralities analysis and verified using published datasets. In total, 720 significantly differentially expressed protein-coding genes were identified in the samples, including 335 upregulated genes and 385 downregulated genes. The upregulated genes were significantly enriched in cell adhesion, biological adhesion and cell-cell adhesion GO terms under biological process (BP). Conversely, the downregulated genes were significantly enriched in embryonic organ morphogenesis, embryonic organ development and embryonic morphogenesis. The KEGG pathway analysis showed that the upregulated genes were enriched in ECM-receptor interaction and focal adhesion pathways. Furthermore, the downregulated genes were enriched in the ErbB, VEGF and MAPK signaling pathways. The PPI network and centralities analysis suggested that ITGA2 and 12 alternate genes were significant hub genes. These findings improve current understanding of the molecular mechanisms underlying HCC development and may be helpful in identifying candidate molecular biomarkers for use in diagnosing, treating and monitoring the prognosis of HCC.
Keywords: development; differentially expressed protein-coding genes; hepatocellular carcinoma; hub gene; transcriptome sequencing.