Centromere Protein F (<i>CENPF</i>) Serves as a Potential Prognostic Biomarker and Target for Human Hepatocellular Carcinoma

Abstract

Overexpression of Centromere Protein F (<i>CENPF</i>) is associated with tumorigenesis of many human malignant tumors. But the molecular mechanism and prognostic value of <i>CENPF</i> in patients with hepatocellular carcinoma (HCC) are still unclear. In this essay, expression of <i>CENPF</i> in HCC tumors were evaluated in a series of databases, including GEO, TCGA, Oncomine, GEPIA, The Human Protein Atlas and Kaplan-Meier plotter. It was apparent that mRNA and protein expression levels of <i>CENPF</i> were significantly increased in patients with HCC and were manifestly associated with the tumor stage of HCC. Aberrant expressions of CENPF were significantly linked with worse overall survival (OS) and progression-free survival (PFS) in HCC patients. Then, immunohistochemistry of <i>CENPF</i> in human HCC samples was carried out to suggest that CENPF protein was over-expressed in HCC tissues, compared with paired adjacent non-cancerous samples. And small interfering RNAs of <i>CENPF</i> in the human HepG2 cells were further performed to reveal that down-regulation of <i>CENPF</i> significantly inhibited cell proliferation, cell migration, and cell invasion, but slightly promoted cell apoptosis in human HepG2 cells. Moreover, the gene-set enrichment analysis (GSEA) was conducted to probe the biology process and molecular signaling pathway of <i>CENPF</i> in HCC. The GSEA analysis pointed out that <i>CENPF</i> was principally enriched in cell cycle and closely related to <i>E2F1</i> and <i>CDK1</i> in the regulation of cell cycle, especially during G2/M transition of mitosis in HCC. Additionally, immune infiltration analysis by CIBERSORTx revealed that mutilpe immune cells, including T_reg, etc., were significantly different in HCC samples with CENPF^high, compared with CENPF^low. These results collectively demonstrated that <i>CENPF</i> might serve as a potential prognostic biomarker and novel therapeutic target for HCC. However, further research is needed to validate our findings and promote the clinical application of <i>CENPF</i> in HCC.