Transcriptome analysis revealed CENPF associated with glioma prognosis

Abstract

<abstract> <p>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.</p> </abstract>

Combined multiomics analysis reveals the mechanism of CENPF overexpression-mediated immune dysfunction in diffuse large B-cell lymphoma in vitro

“…Furthermore, it was interesting that the significantly increased proteins were mainly enriched with various ubiquitination-related enzymes, which was revealed by functional enrichment. This finding was consistent with previous findings that CENPF participates in ubiquitin-mediated proteolysis in cancer (Shi and Zhang, 2017;Zhang et al, 2021).…”

“…The expression of CENPF in GO/Gl-cells is low, and it accumulates in the nuclear matrix during S-phase, with the maximum level in G2/M-cells (Liao et al, 1995). At present, CENPF is generally considered a potential marker of proliferation in a variety of malignant tumors, as it is elevated in various malignant tumors, such as liver cancer (Huang et al, 2021), gastric carcinoma (Chen et al, 2019), lung cancer (Li et al, 2021), breast cancer (Chen et al, 2020), prostate cancer (Shahid et al, 2019) and malignant glioma (Zhang et al, 2021) and is associated with poor prognosis in patients. In 2005, a radio-immunological assay was used to compare 347 non-Hodgkin's lymphoma patients and 150 control subjects, and the proportions of CENPF detected in the two groups were 7.2% and 1.3% (p < 0.05), respectively, suggesting that CENPF may play a role in the development and progression of some types of NHL (Bencimon et al, 2005).…”

Single‐cell RNA sequencing reveals tumor heterogeneity, microenvironment, and drug‐resistance mechanisms of recurrent glioblastoma

“…Furthermore, we observed extensive intratumoral heterogeneity at the transcriptional level; the CNV phenotypes were different between reference cells and observation cells, and cell subtype ratios were different in patients with recurrent GBM. Moreover, we identified cluster 12 mainly including dividing OPCs, which were characterized by high expression of genes encoding proliferation‐related proteins that were negatively associated with the prognosis of patients with glioma, as previously reported 37–40 …”

“…Moreover, we identified cluster 12 mainly including dividing OPCs, which were characterized by high expression of genes encoding proliferation-related proteins that were negatively associated with the prognosis of patients with glioma, as previously reported. [37][38][39][40] The GBM TME consists of a heterogeneous cellular milieu that can influence cancer cell behavior. Genomic alterations can reshape the TME to drive tumor malignancy.…”

The Epigenetic Evolution of Glioma Is Determined by the IDH1 Mutation Status and Treatment Regimen

“…Interestingly, of those, 83 genes have been previously experimentally identified by ChIP-seq as HOXD13 target in human or mouse, according to the ChEA ( 39 ) and CISTROME ( 40 ) databases and are upregulated in our IDHmut-noncodel transcriptomic cohort ( N = 23 paired samples; Supplementary Table S4C), while no changes were observed in the IDHmut-codel cohort (data not shown). Some of these HOXD13 targets are well-established oncogenes related to cell proliferation: Centromere protein F (CENPF) has been described to enhances the progression of adrenocortical carcinoma ( 62 ) and was associated to poor prognosis in breast cancer ( 63 ) and gliomas ( 64 ); Proliferating cell nuclear antigen (PCNA) has been reported as a prognostic indicator in gliomas ( 65, 66 ) and has been tested as a potential target to inhibit tumor cell proliferation ( 67 ); Homeobox protein A7 (HOXA7) has been reported to promote tumor growth and metastasis in liver cancer ( 68 ).…”