CDK1 serves as a novel therapeutic target for endometrioid endometrial cancer
Xue Ying1, Xuan Che1,2, Jianzhang Wang1
1Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, P.R. China, 310006.
Abstract:
Background: Endometrial cancer (EC) is one of the most common and prevalent gynecologic malignancies worldwide. The aim of this study was to identify a novel therapeutic target for endometrioid endometrial cancer. Materials and Methods: Bioinformatic analysis was performed and CDK1 was screen out as one of the hub genes in the pathogenesis of EC. Immunohistochemistry was used to verify the expression of CDK1 in endometrial cancer tissue. Cell viability and colony formation were used to study the effects of CDK1 on the proliferation and colony formation of endometrial cancer cells in vitro. Apoptosis and cell cycle assays were used to elucidate the mechanism of CDK1 affecting cell proliferation. Tumor xenograft transplantation assay was performed to show the effects of CDK1 on the growth of endometrial cancer cells in vivo. Results: CDK1 was over expressed in endometrioid endometrial cancer, and accumulation of cytoplasmic CDK1 was associated with histological grade of EC. CDK1 promoted endometrial cancer cell growth and colony formation in vitro. The inhibition of CDK1 activity induced cell apoptosis and caused G2/M phase arrest of cell cycle in endometrial cancer cells. The inhibition of CDK1 activity also inhibited endometrial cancer growth in xenograft models. Conclusion: CDK1 was involved in the pathogenesis of endometrioid endometrial cancer and provided a novel therapeutic target for endometrioid endometrial cancer.
Insights
Cyclin-dependent kinase 1 (CDK1) promotes endometrioid endometrial cancer growth. Inhibiting CDK1 induces apoptosis and halts cancer progression, identifying CDK1 as a potential therapeutic target for this malignancy.
Area of Science:
- Oncology
- Molecular Biology
- Gynecologic Oncology
Background:
- Endometrial cancer (EC) is a prevalent gynecologic malignancy globally.
- Identifying novel therapeutic targets is crucial for improving patient outcomes in endometrioid EC.
- CDK1 emerged as a key gene in EC pathogenesis through bioinformatic analysis.
Purpose of the Study:
- To investigate the role of CDK1 in endometrioid endometrial cancer.
- To evaluate CDK1 as a potential therapeutic target for EC.
Main Methods:
- Bioinformatic analysis to identify hub genes.
- Immunohistochemistry to assess CDK1 expression in EC tissues.
- In vitro cell assays (viability, colony formation, apoptosis, cell cycle) to determine CDK1's functional role.
- In vivo xenograft models to evaluate therapeutic efficacy.
Main Results:
- CDK1 is overexpressed in endometrioid EC, with cytoplasmic accumulation correlating with histological grade.
- CDK1 promotes EC cell proliferation and colony formation in vitro.
- CDK1 inhibition leads to apoptosis and G2/M cell cycle arrest in EC cells.
- Inhibition of CDK1 suppresses tumor growth in vivo.
Conclusions:
- CDK1 plays a significant role in the pathogenesis of endometrioid endometrial cancer.
- CDK1 represents a promising novel therapeutic target for endometrioid EC treatment.
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