ArticleHereditas2025
Mechanistic insights into CDCA gene family-mediated glioblastoma progression: implications for diagnosis, prognosis, and therapeutic targeting.
Article in Hereditas, 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
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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.
- MYBL2 promotes malignant phenotypes and M2-like macrophage polarization through CCL2 in non-small cell lung cancer.Molecular and cellular biochemistry · 2026Article
- Role of cell division cycle associated 2 in ovarian cancer: Effects on tumor progression and cisplatin resistance.CytoJournal · 2025Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GBM) is a highly aggressive brain tumor characterized by poor prognosis and limited therapeutic options. Understanding the molecular mechanisms driving GBM progression is essential for developing more effective diagnostic and therapeutic approaches. Specifically, investigating Cell Division Cycle-Associated (CDCA) genes offers new perspectives on cell cycle regulation and the proliferation of GBM cells, which are key factors in tumor growth and resistance to treatment. These genes have not been extensively studied in GBM, making them a promising area for targeted research and potential therapeutic interventions. This project was launched to elucidate the pathogenic, diagnostic, and therapeutic roles of CDCA genes in GBM. METHODOLOGY: Total RNA was extracted from GBM cell lines followed by RT-qPCR to analyze the expression of CDCA genes. The expression validation, prognostic significance, and mutational analysis of CDCA genes were performed using various databases. Functional assays, including gene knockdown, colony formation, proliferation, and wound healing, were conducted in U87MG cells to assess the role of CDCA7 and CDCA8 in GBM.
resultsThe expression analysis of CDCA genes in 12 GBM cell lines and 6 normal brain cell lines revealed significant overexpression of these genes in GBM. ROC curve analysis demonstrated excellent diagnostic potential, with AUC values of 1 for most genes. This indicates that CDCA gene expression effectively distinguishes GBM cells from normal brain cells. Validation using additional TCGA data confirmed the upregulation of these genes in GBM tumors, with significant association to key cancer-related pathways. Survival analysis showed that higher expression of CDCA genes correlated with poor prognosis in GBM patients. Mutation, CNV, and methylation analyses revealed alterations in these genes, further supporting their role in GBM. Additionally, CDCA gene expression was linked to immune modulation and cell cycle-related functions, suggesting their involvement in immune evasion and tumor proliferation. Knockdown experiments of CDCA7 and CDCA8 in U87MG cells demonstrated a reduction in cell proliferation, colony formation, and migration, highlighting their potential as therapeutic targets.
conclusionOverall, our findings suggest that CDCA genes could serve as both diagnostic biomarkers and therapeutic targets for GBM.
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