Transcriptome analysis revealed CENPF associated with glioma prognosis

Gliomas are common malignant tumors of the central nervous system. Despite the surgical resection and postoperative radiotherapy and chemotherapy, the prognosis of glioma remains poor. Therefore, it is important to reveal the molecular mechanisms that promotes glioma progression. Microarray datasets were obtained from the Gene Expression Omnibus (GEO) database. The GEO2R tool was used to identify 428 differentially expressed genes (DEGs) and a core module from three microarray datasets. Heat maps were drawn based on DEGs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed using the DAVID database. The core module was significantly involved in several KEGG pathways, such as "cell cycle", "viral carcinogenesis", "progesterone-mediated oocyte maturation", "p53 signaling pathway". The protein-protein interaction (PPI) networks and modules were built using the STRING database and the MCODE plugin, respectively, which were visualized using Cytoscape software. Identification of hub genes in the core module using the CytoHubba plugin. The top modular genes AURKA, CDC20, CDK1, CENPF, and TOP2A were associated with glioma development and prognosis. In the Human Protein Atlas (HPA) database, CDC20, CENPF and TOP2A have significant protein expression. Univariate and multivariate cox regression analysis showed that only CENPF had independent influencing factors in the CGGA database. GSEA analysis found that CENPF was significantly enriched in the cell cycle, P53 signaling pathway, MAPK signaling pathway, DNA replication, spliceosome, ubiquitin-mediated proteolysis, focal adhesion, pathway in cancer, glioma, which was highly consistent with previous studies. Our study revealed a core module that was highly correlated with glioma development. The key gene CENPF and signaling pathways were identified through a series of bioinformatics analysis. CENPF was identified as a candidate biomarker molecule.