CDK1-PLK1/SGOL2/ANLN pathway mediating abnormal cell division in cell cycle may be a critical process in hepatocellular carcinoma

This study aims to investigate the potential mechanisms and identify core biomarkers of Hepatocellular carcinoma (HCC). The profile GSE113850 was downloaded to analyze the differentially expressed genes. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction network analysis were used to reveal the main signal pathways of the differentially expressed genes (DEGs) and hub genes. The correlation between core gene expression and pathological stages, the disease-free survival analysis, the overall survival analysis were analyzed by Gene Expression Profiling Interactive Analysis. Furthermore, we reidentified the expression level of core genes of carcinoma tissues and para-carcinoma tissues from 14 HCC patients with real-time reverse transcription-polymerase chain reaction analysis (RT-PCR) and western blotting. After SK-Hep1 cell was treated with cyclin-dependent kinase 1 (CDK1) siRNA for 72 h, we detected the expression of the core genes and fluorescence-activated cell sorting analysis. A total of 378 DEGs were found. GO and KEGG analysis revealed that the DEGs were mainly enriched in the cell cycle. There were positive correlations among CDK1, polo-like kinase 1, shugoshin2 and anillin actin-binding protein. Moreover, the expression levels of four core genes were related to the HCC occurrence, pathological stages, and survivorship curve. The clinical HCC specimens verified the higher expression level of core genes by real-time RT-PCR. The transfection of siCDK1 in SK-Hep1 resulted in a disordered cell cycle. Furthermore, CDK1 knockdown suppressed the expression of PLK1, ANLN, and SGOL2. The CDK1-PLK1/SGOL2/ANLN pathway mediating abnormal cell division in the cell cycle might be a critical process in HCC.