ArticleJournal of gynecologic oncology2024
CDK1 promotes the phosphorylation of KIFC1 to regulate the tumorgenicity of endometrial carcinoma.
Article in Journal of gynecologic oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- The Clinical Significance of KIFs in Cervical and Endometrial Cancer: from Mechanisms to Biomarker and Therapeutic Potential.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Hispidulin Suppresses Hepatocellular Carcinoma Proliferation by Targeting PI3K-Akt Pathway: A Network Pharmacology and Experimental Validation Study.Journal of hepatocellular carcinoma · 2026Article
- Post-Translational Modifications of Proteins Orchestrate All Hallmarks of Cancer.Life (Basel, Switzerland) · 2025Review
- KIF18A and CDK1 as combined therapeutic targets in cervical and endometrial carcinomas: based on bioinformatics analysis andTranslational cancer research · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
objectiveThis study aims to clarify the mechanical action of cyclin-dependent protein kinase 1 (CDK1) in the development of endometrial carcinoma (EMCA), which may be associated with the phosphorylation of kinesin family member C1 (KIFC1) and further activate the PI3K/AKT pathway.
methodsThe protein and gene expression of CDK1 in EMCA tissues and tumor cell lines were evaluated by western blot, quantitative polymerase chain reaction, and immunohistochemistry staining. Next, Cell Counting Kit-8 and colony formation assay detected cell survival and proliferation. Cell migration and invasion were measured by Transwell assay. Cell apoptosis and cell cycle were tested by flow cytometry. Immunofluorescence staining of γH2AX was used to evaluate DNA damage, respectively. Subsequently, a co-immunoprecipitation assay was used to detect the interaction between CDK1 and KIFC1. The phosphorylated protein of KIFC1 and PI3K/AKT was detected by western blot. Finally, the effect of CDK1 on the tumor formation of EMCA was evaluated in a nude mouse xenograft model.
resultsCDK1 was highly expressed in EMCA tumor cell lines and tissues, which contributed to cell survival, proliferation, invasion, and migration, inhibited cell apoptosis, and induced DNA damage of EMCA cells dependent on the phosphorylation of KIFC1. Moreover, the CDK1-KIFC1 axis further activated PI3K/AKT pathway. Finally, CDK1 knockdown repressed tumor formation of EMCA in vivo.
conclusionWe report that increased CDK1 promotes tumor progression and identified it as a potential prognostic marker and therapeutic target of EMCA.
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