ArticleJournal of cancer research and clinical oncology2025
CENPF as a prognostic marker of glioma: unraveling the molecular mechanisms.
Article in Journal of cancer research and clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- KIF23 in disease pathogenesis and therapeutics : from molecular mechanisms to clinical translation.Cancer cell international · 2026Review
- CENPF Overexpression Induced by HBV Infection Facilitates the G1/S Cell Cycle Transition of Hepatocellular Carcinoma Cells via MYC Pathway.Journal of hepatocellular carcinoma · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveGlioma is the dominant primary intracranial malignancy. The roles of CENPF and the CENPF - p53 axis in glioma remain elusive. This study uses bioinformatics and animal experiments to clarify the relationship between CENPF and p53 in glioma. CENPF affects spindle assembly and chromosomal segregation, while p53 is a tumor-suppressor gene. Their dysregulation may interact and impact glioma development. Our research aims to uncover the underlying molecular mechanisms, offering new perspectives for glioma diagnosis and treatment.
methodGene expression data from the Gene Expression Omnibus (GEO) database ( http://www.ncbi.nlm.nih.gov/geo/ ) were retrieved, specifically datasets GSE50161, GSE104291, and GSE12249. Volcano plots were generated to visualize differentially expressed genes (DEGs), and intersecting DEGs were identified using Venn diagrams. Weighted gene co-expression network analysis (WGCNA) was employed to construct and analyze the protein-protein interaction (PPI) network. Additionally, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted. Gene set enrichment analysis (GSEA) was utilized for comprehensive GO and KEGG analyses of the entire genome. Comparative Toxicogenomics Database (CTD) analysis was performed, and TargetScan was used to identify miRNAs regulating central DEGs. An animal model of glioma was established and analyzed via Western blot.
resultA total of 501 differentially expressed genes (DEGs) were identified, from which eight significant modules were generated and ten core genes were extracted. These core genes exhibited differential expression patterns between glioma tumor and non-tumor samples. Expression analysis revealed that the ten core genes associated with glioma (CENPF, PBK, ASPM, KIF2C, KIF20A, CDC20, TOP2A, NUSAP1, TTK, KIF23) were significantly upregulated in tumor tissues (P < 0.05). They are primarily enriched in protein signal transduction, coated membrane structures, AP-type membrane coat adaptor complexes, and chloride channel activity. KEGG pathway analysis indicated that these target genes were mainly involved in nicotine addiction, arginine and proline metabolism, beta-alanine metabolism, and histidine metabolism. The mouse model confirmed that CENPF and CDK-1 were highly expressed in glioma tissues, while p53, p21, and Caspase9 were downregulated, leading to inhibition of the apoptosis pathway and exacerbation of glioma progression. Overexpression of CENPF further suppressed key molecules in the p53-mediated apoptosis pathway. Conversely, low expression of CENPF activated these key molecules, inducing apoptosis in glioma cells.
conclusionsCENPF exhibits elevated expression levels in glioma, potentially inhibiting cell apoptosis via the p53 signaling pathway, consequently contributing to the onset and progression of glioma.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.