MiR‑495‑3p and miR‑143‑3p co‑target CDK1 to inhibit the development of cervical cancer

• J. Tang ^[1] ; H. Pan ^[2] ; W. Wang ^[3] ; C. Qi ^[3] ; C. Gu ^[4] ; A. Shang ^[3] ; J. Zhu ^[5]
  1. [1] Department of Gynecology and Obstetrics, Huzhou Central Hospital, Affiliated Central Hospital of Huzhou Normal University, Huzhou 313003, People’s Republic of China
  2. [2] Department of Laboratory Medicine, Shanghai Simple Gene Medical Laboratory, Shanghai 200025, People’s Republic of China
  3. [3] Department of Pathology, The Sixth People’s Hospital of Yancheng City, Yancheng 224005, People’s Republic of China
  4. [4] Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, People’s Republic of China
  5. [5] Department of Laboratory Medicine, Huzhou Central Hospital, Affiliated Central Hospital of Huzhou Normal University, Huzhou 313003, Zhejiang Province, People’s Republic of China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 23, Nº. 11, 2021, págs. 2323-2334
• Idioma: inglés
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• Resumen

  • 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 develop- ment of cervical cancer.