ArticleDiscover oncology2025
Suppressing CDCA8/CDK1 improves oral squamous cell carcinoma by modulating proliferation, apoptosis, cell cycle and migration.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Authors and funding
7 authors.
Funding
Abstract
We aimed to clarify the role of CDCA8/CDK1 in the progression of oral squamous cell carcinoma (OSCC) and the potential mechanisms. To explore the CDCA8 expression in OSCC, clinical samples were collected. In vitro, CAL-27 cells were transfected with short hairpin RNA (shRNA) to silence CDCA8, and then proliferation, apoptosis, cell cycle and migration were evaluated. KEGG analysis was used to explore the causal association of CDCA8 and CDK1 during the development of OSCC. CDK1 inhibitor RO3306 and overexpression of CDK1 were used to clarify the regulatory role of CDK1 in OSCC. In vivo, mice were injected with shCDCA8 to deplete CDCA8 based on establishing a model of OSCC. We found that CDCA8 was highly expressed in OSCC tissues and cell lines. In vitro experiments, suppressing CDCA8 in CAL-27 cells improved OSCC, characterized by increased apoptosis and decreased proliferation and migration. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that cell cycle formed a direct interaction with CDCA8 and inhibition of CDCA8 efficiently reduced levels of CDK1 and CDK2. Additional experiments showed that CDCA8-activated CDK1 was the key regulator of OSCC. In vivo, we verified that depletion of CDCA8 inhibited proliferation and metastasis of OSCC. CDCA8-activated CDK1 acts a crucial role in the development of OSCC by modulating cell growth, migration, and metastasis.
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Registered trials
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