ArticleFuture science OA2026
Multi-omics profiling identifies CDK1 as a key mediator of mitosis through the PTN pathway in bladder cancer.
Article in Future science OA, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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11 authors.
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Abstract
aimsThis study aimed to characterize cyclin-dependent kinase 1 (CDK1) expression in bladder cancer (BC), elucidate its role in intercellular signaling and mitosis, and identify small-molecule inhibitors targeting CDK1.
methodsRNA sequencing data from multiple databases were integrated, with immunohistochemistry on tissue microarrays validating protein expression. Single-cell RNA sequencing (scRNA-seq), spatial transcriptomics (ST), gene set enrichment analysis (GSEA), and molecular docking with molecular dynamics (MD) simulations were performed.
resultsCDK1 mRNA and protein were significantly overexpressed in BC tissues. CDK1 expression correlated with patient age and race. CDK1 was predominantly expressed in epithelial cells and central to pleiotrophin (PTN) pathway-mediated intercellular communication; virtual CDK1 knockout markedly reduced PTN signaling strength. ST confirmed CDK1 enrichment in tumor regions. GSEA linked CDK1 to mitosis and chromosome segregation, and scRNA-seq analyses revealed a PTN-CDK1-mitosis regulatory axis active specifically in epithelial cells. Dinaciclib showed favorable MD stability as a CDK1 inhibitor.
conclusionCDK1 is significantly overexpressed in BC with good discriminatory ability. Predominantly expressed in BC epithelial cells, CDK1 may be activated by PTN signaling to drive mitosis. MD simulations support Dinaciclib as a promising CDK1-targeting inhibitor.
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