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Updated: Oct 24, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-495-3p and miR-143-3p co-target CDK1 to inhibit the development of cervical cancer
1Department of Gynecology and Obstetrics, Huzhou Central Hospital, Affiliated Central Hospital of Huzhou Normal University, Huzhou, 313003, People's Republic of China.
Purpose:
The GEO database and KEGG database-based analyses identified the differential expression of cyclin-dependent kinase 1 (CDK1) in cervical cancer and its involvement in the cell cycle pathway. In the present study, we aim to clarify the role of CDK1 in cervical cancer and the function of upstream microRNA (miR)-143-3p/miR-495-3p.
Methods:
The expression of miR-143-3p, miR-495-3p, and CDK1 in cervical cancer tissues and cells was determined using RT-qPCR. Cell bioactivities were examined by CCK-8 and flow cytometry. The binding affinity between CDK1 and miR-143-3p/miR-495-3p was investigated using dual luciferase gene reporter assay. A xenograft mouse model of cervical cancer was then established to explore their effect on the tumorigenicity of cervical cancer cells in vivo.
Results:
CDK1 was found to be the common target gene of miR-143-3p and miR-495-3p. CDK1 overexpression occurred in cervical cancer tissues and cells, while expression of miR-495-3p and miR-143-3p was down-regulated. The viability was inhibited while the apoptosis was promoted in cervical cancer cells in response to miR-143-3p or miR-495-3p overexpression, or CDK1 silencing. Further, miR-143-3p or miR-495-3p overexpression was also substantiated to inhibit the tumorigenicity of cervical cancer cells in vivo, while CDK1 overexpression counteracted their effect.
Conclusion:
Taken together, miR-143-3p and miR-495-3p co-target CDK1, thereby inhibiting the occurrence and development of cervical cancer.
Insights
MicroRNA-143-3p and microRNA-495-3p target cyclin-dependent kinase 1 (CDK1) in cervical cancer. Their co-targeting inhibits cervical cancer cell viability and tumorigenicity, suggesting a therapeutic role.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cyclin-dependent kinase 1 (CDK1) is implicated in cervical cancer progression via cell cycle regulation.
- MicroRNAs (miRNAs) are key regulators of gene expression and can act as tumor suppressors or oncogenes.
Purpose of the Study:
- To elucidate the role of CDK1 in cervical cancer.
- To investigate the regulatory function of upstream microRNA (miR)-143-3p and miR-495-3p on CDK1 in cervical cancer.
Main Methods:
- Quantitative reverse transcription PCR (RT-qPCR) to assess miRNA and CDK1 expression.
- Cell counting kit-8 (CCK-8) and flow cytometry for cell viability and apoptosis assays.
- Dual luciferase reporter assay to confirm direct targeting.
- In vivo xenograft mouse model to evaluate tumorigenicity.
Main Results:
- CDK1 is a common target of miR-143-3p and miR-495-3p.
- CDK1 was overexpressed, while miR-143-3p and miR-495-3p were downregulated in cervical cancer tissues and cells.
- Overexpression of miR-143-3p or miR-495-3p, or CDK1 silencing, inhibited cell viability and promoted apoptosis.
- In vivo, miR-143-3p/miR-495-3p overexpression suppressed tumor growth, an effect counteracted by CDK1 overexpression.
Conclusions:
- miR-143-3p and miR-495-3p act as tumor suppressors in cervical cancer by co-targeting CDK1.
- This miRNA-CDK1 axis plays a crucial role in inhibiting cervical cancer occurrence and development.
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