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Centrosomes, genomic instability, and cervical carcinogenesis.

Stefan Duensing1, Karl Münger

  • 1Harvard Medical School, Department of Pathology, Armenise 537, 200 Longwood Avenue, Boston, MA 02115, USA. stefan_duensing@hms.harvard.edu

Critical Reviews in Eukaryotic Gene Expression
|July 4, 2003
PubMed
Summary

High-risk human papillomavirus (HPV) oncoproteins E6 and E7 drive cervical cancer by causing genomic instability and abnormal cell division. These oncoproteins disrupt centrosome function, leading to chromosomal abnormalities early in tumor development.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cervical cancer development is strongly linked to high-risk human papillomavirus (HPV) infection.
  • Genomic instability, particularly aneuploidy, is a hallmark of cancer and is observed early in cervical precursor lesions.
  • Abnormal cell division, indicated by multipolar mitotic figures, suggests defects in chromosome segregation during cervical carcinogenesis.

Purpose of the Study:

  • To investigate the distinct mechanisms by which high-risk HPV E6 and E7 oncoproteins induce centrosome abnormalities.
  • To explore the functional consequences of these distinct mechanisms on genomic instability.
  • To understand the synergistic effects of HPV E6 and E7 co-expression on chromosomal instability.

Main Methods:

  • Analysis of high-risk HPV-encoded oncoproteins E6 and E7 in cervical carcinogenesis models.

Related Experiment Videos

  • Assessment of centrosome duplication and number in cells expressing E6 or E7.
  • Evaluation of multinucleation, nuclear atypia, and mitotic figures in relation to HPV oncoprotein expression.
  • Investigation of the interplay between E6 and E7 pathways in driving genomic instability.

    • Main Results:

    • High-risk HPV E7 oncoprotein targets the pRB pathway, causing abnormal centrosome duplication in otherwise normal cells.
    • High-risk HPV E6 oncoprotein inactivates p53, leading to increased centrosome numbers, multinucleation, and nuclear atypia.
    • Co-expression of HPV E6 and E7 demonstrates synergistic effects on centrosome abnormalities and chromosomal instability.
    • Chromosomal instability arises as a direct consequence of oncogenic insults during early tumor progression.

    Conclusions:

    • High-risk HPV E6 and E7 oncoproteins induce centrosome abnormalities through distinct molecular pathways.
    • These distinct pathways contribute to genomic instability and chromosomal defects crucial for cervical carcinogenesis.
    • The findings support a model where oncogenic insults directly cause chromosomal instability early in cancer development.