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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.9
- 수록면
- 1 - 17 (17page)
- DOI
- https://doi.org/10.3802/jgo.2024.35.e68
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초록· 키워드
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Objective: This study aims to clarify the mechanical action of cyclin-dependent proteinkinase 1 (CDK1) in the development of endometrial carcinoma (EMCA), which may beassociated with the phosphorylation of kinesin family member C1 (KIFC1) and furtheractivate the PI3K/AKT pathway.
Methods: The protein and gene expression of CDK1 in EMCA tissues and tumor celllines were evaluated by western blot, quantitative polymerase chain reaction, andimmunohistochemistry staining. Next, Cell Counting Kit-8 and colony formation assaydetected cell survival and proliferation. Cell migration and invasion were measuredby 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 betweenCDK1 and KIFC1. The phosphorylated protein of KIFC1 and PI3K/AKT was detected bywestern blot. Finally, the effect of CDK1 on the tumor formation of EMCA was evaluated in anude mouse xenograft model.
Results: CDK1 was highly expressed in EMCA tumor cell lines and tissues, which contributedto cell survival, proliferation, invasion, and migration, inhibited cell apoptosis, and inducedDNA damage of EMCA cells dependent on the phosphorylation of KIFC1. Moreover, theCDK1-KIFC1 axis further activated PI3K/AKT pathway. Finally, CDK1 knockdown repressedtumor formation of EMCA in vivo.
Conclusion: We report that increased CDK1 promotes tumor progression and identified it asa potential prognostic marker and therapeutic target of EMCA.
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