Hepatocellular carcinoma (HCC) is the most aggressive type of gastrointestinal tumor, with a high rate of mortality. However, identifying biomarkers for the treatment of HCC remains to be developed. We aimed to determine whether cell division cycle 25C (CDC25C) could be used as a novel diagnostic and therapeutic biomarker in HCC. Expression of CDC25C in HCC was analyzed by using GEPIA (Gene Expression Profiling Interactive Analysis) and UALCAN databases. GEPIA and CBioPortal databases were applied to analyze patients’survival and CDC25C mutations, respectively. PPI (Protein-Protein Interaction) network was further built by STRING (Search Tool for the Retrieval of Interacting Genes) and Metascape Web portals. To the best of our knowledge, the novel observations identified in the present study reveal that the expression of CDC25C in HCC was significantly enhanced when compare to that in normal liver tissues (P < 0.001). A higher CDC25C expression resulted in a remarkably shorter disease free survival as well as overall survival. Moreover, the expression of CDC25C in HCC was related to HCC patients’grade and race, but not gender. The expression levels of CDC25C elevated gradually from stage 1 to 3 but decreased in stage 4. The specific gene mutations V41A, L87 H, N222 K and X309-splice of CDC25C occurred in HCC samples and these unique mutations were not detected in any other tumor tissues. Finally, PPI networks and GO enrichment analysis suggested that CDC25C might be associated with cell cycle and p53 signaling pathway. Taken together, bioinformatics analysis revealed that CDC25C might be a potential diagnostic predictor for HCC.

We aimed to identify if PLK1 could be used as a new diagnostic and therapeutic biomarker in hepatocellular carcinoma (HCC) patient. Expression of PLK1 in HCC was analyzed by using GEPIA (Gene Expression Profiling Interactive Analysis) and UALCAN databases. GEPIA and CBioPortal tools were applied to determine patients' survival and PLK1 mutations, respectively. PPI (Protein-Protein Interaction) networks were further built by STRING (Search Tool for the Retrieval of Interacting Genes) and Metascape Web portals. The data demonstrated that the expression of PLK1 in HCC was significantly enhanced when compared to normal liver tissues (P < 0.001). A higher PLK1 expression resulted in a remarkably shorter disease-free survival as well as overall survival. Moreover, the expression of PLK1 in HCC was related to HCC patients' grade and race, but not gender. The data also suggested that expression of PLK1 elevated gradually from stage 1 to 3 but decreased in stage 4. Three specific gene mutations K146R, S335Afs*120 and D429H of PLK1 occurred in HCC and these unique mutations were not seen in any other tumor tissues. Finally, PPI networks and GO enrichment analysis suggested that PLK1 might be associated with cell cycle and p53 signaling pathway etc. Taken together, our novel findings suggest that PLK1 is implicated in the poor prognosis of hepatocellular carcinoma.