ArticlePloS one2026
Multi-omics analysis identifies CCNB1 as a cell cycle factor driving glioblastoma progression and its inhibition by resveratrol.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed.
- GDPPH1 induces cell cycle arrest by downregulation of CDK4/Cyclin D1 via the mCell death & disease · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is a fast-growing primary brain tumor with high mortality and recurrence rates. Dysregulation of the cell cycle is a hallmark of GBM, and cyclin B1 (CCNB1) is a key regulator of the cell cycle. However, the role of CCNB1 in GBM remains unclear. In this study, we found that CCNB1 mRNA and protein expression levels were significantly higher in GBM tissues than normal tissues. High CCNB1 mRNA expression was associated with poorer prognosis in GBM patients. Single-cell and spatial transcriptomics data revealed that CCNB1+ cells represent a proliferative subcluster in GBM, annotated as proliferative cells, and characterized by the upregulation of cell cycle-related pathways. CCNB1 inhibition decreased the proliferation of GBM cells and impaired cell cycle progression from S phase to G2/M. Additionally, resveratrol could inhibit the expression of CCNB1 and its interacting gene polo-like kinase 1 (PLK1). Importantly, through in vitro and in vivo experiments, we found that resveratrol suppressed GBM cell growth with low toxicity. CCNB1 silencing combined with resveratrol treatment further inhibited the proliferation of GBM cells. Collectively, these data suggest that CCNB1 is highly expressed in GBM and may promote GBM progression. Inhibition of CCNB1 may represent a potential therapeutic strategy for GBM.
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Registered trials
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