Related Experiment Video

Updated: Jul 6, 2026

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

Published on: February 25, 2016

Multi-omics profiling identifies CDK1 as a key mediator of mitosis through the PTN pathway in bladder cancer

Li Yang1, Jia-Ming Zhang1, Yu-Jia Chen2

  • 1Department of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, P. R. China.

Future Science OA
|July 4, 2026
PubMed
Abstract

Insights

Cyclin-dependent kinase 1 (CDK1) is overexpressed in bladder cancer (BC) and drives mitosis via PTN signaling. Dinaciclib shows promise as a CDK1 inhibitor for BC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Bladder cancer (BC) is a significant health concern with complex molecular underpinnings.
  • Understanding key regulatory proteins like cyclin-dependent kinase 1 (CDK1) is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the expression and function of CDK1 in BC.
  • To explore CDK1's role in intercellular signaling and mitosis.
  • To identify potential small-molecule inhibitors targeting CDK1 for BC treatment.

Main Methods:

  • Integrated RNA sequencing data with immunohistochemistry for protein validation.
  • Utilized single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST).
  • Performed gene set enrichment analysis (GSEA) and molecular dynamics (MD) simulations for inhibitor assessment.

Main Results:

  • CDK1 mRNA and protein were significantly overexpressed in BC tissues, correlating with patient demographics.
  • CDK1 plays a central role in PTN pathway-mediated intercellular communication and mitosis.
  • Spatial transcriptomics confirmed CDK1 enrichment in tumor regions, revealing a PTN-CDK1-mitosis axis in epithelial cells.

Conclusions:

  • CDK1 overexpression in BC has strong discriminatory potential.
  • CDK1, activated by PTN signaling in BC epithelial cells, drives mitosis.
  • Molecular dynamics simulations suggest Dinaciclib as a viable CDK1 inhibitor for BC therapy.
Keywords:
CDK1bladder cancercellular communicationmitosistargeted therapy

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