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[Early Mitotic Inhibitor 1 Regulates DNA Re-replication Mediated by Human Papillomavirus Subtype 16 E7 in Response to

Ya-Fei Liu, Yan-Jun Shen, Yang Yang

    Zhongguo Yi Xue Ke Xue Yuan Xue Bao. Acta Academiae Medicinae Sinicae
    |September 8, 2020
    PubMed

    Insights

    Human papillomavirus subtype 16 E7 oncogene drives DNA re-replication after DNA damage. Early mitotic inhibitor 1 (Emi1) promotes this process, and its inhibition reduces polyploidy in HPV-16 E7 cells.

    Area of Science:

    • Molecular biology
    • Oncology
    • Virology

    Background:

    • Human papillomavirus subtype 16 (HPV-16) is a major cause of cervical cancer.
    • The HPV-16 E7 oncogene plays a critical role in viral carcinogenesis.
    • Understanding the molecular mechanisms of HPV-16 E7-induced genomic instability is crucial.

    Purpose of the Study:

    • To investigate the role of HPV-16 E7 oncogene in DNA re-replication following DNA damage.
    • To elucidate the molecular mechanism by which HPV-16 E7 induces DNA re-replication.
    • To examine the involvement of Early mitotic inhibitor 1 (Emi1) in this process.

    Main Methods:

    • Stable expression of HPV-16 E7 in RPE1 cells.
    • Flow cytometry to analyze cell cycle progression and polyploidy.
    • Immunoblotting to assess Emi1 protein levels.
    • RNA interference to inhibit Emi1 expression.

    Main Results:

    • HPV-16 E7 expression significantly increased polyploidy in response to DNA damage.
    • Emi1 protein levels were elevated in DNA-damaged RPE1 E7 cells.
    • Interference with Emi1 using small interfering RNAs reduced the polyploid ratio in HPV-16 E7 cells.

    Conclusions:

    • HPV-16 E7 oncogene induces DNA re-replication upon DNA damage.
    • Emi1 is a key mediator promoting HPV-16 E7-driven DNA re-replication.
    • Targeting Emi1 may offer a strategy to counteract HPV-16-associated genomic instability.
    Keywords:
    DNA re-replicationE7early mitotic inhibitor 1human papillomavirus-16

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