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Human papillomavirus E6 and E7: proteins which deregulate the cell cycle

M Tommasino1, L Crawford

  • 1Department of Pathology, University of Cambridge, UK.

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|June 1, 1995
PubMed
Summary

Human Papillomaviruses (HPV) are linked to genital tract cancers. HPV E6 and E7 proteins disrupt tumor suppressor genes p53 and Rb1, causing cell cycle deregulation and promoting cancer development.

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Clinical, epidemiological, and molecular data link Human Papillomaviruses (HPV) to genital tract cancers.
  • HPV shares transformation pathways with DNA tumor viruses like Adenovirus and SV40, but is uniquely implicated in human cancers.
  • Extensive research implicates HPV E6 and E7 oncoproteins in malignant transformation.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which HPV E6 and E7 proteins contribute to cancer development.
  • To understand the interaction between HPV oncoproteins and critical host cell cycle regulators.

Main Methods:

  • Review of existing clinical, epidemiological, and molecular findings.
  • Analysis of the functional interactions between HPV E6/E7 proteins and tumor suppressor proteins p53/Rb1.

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  • Examination of the impact on cell cycle control, DNA replication, DNA repair, and apoptosis.

    • Main Results:

    • HPV E6 protein binds and inactivates the p53 tumor suppressor protein.
    • HPV E7 protein binds and inactivates the Rb1 tumor suppressor protein.
    • These interactions lead to cell cycle deregulation, loss of control over DNA replication, repair, and apoptosis, facilitating malignant transformation.

    Conclusions:

    • HPV's oncogenic potential is mediated by the E6 and E7 proteins.
    • Disruption of p53 and Rb1 pathways by HPV is a key step in the development of HPV-associated cancers.
    • Understanding these molecular interactions is crucial for developing targeted cancer prevention and therapies.