Abstract
The high-risk strains of human papillomavirus (HR-HPV) are known to be causative agents of cervical cancer and have recently also been implicated in cancers of the oropharynx. E6 is a potent oncogene of HR-HPVs, and its role in the progression to malignancy has been and continues to be explored. E6 is known to interact with and subsequently inactivate numerous cellular proteins pivotal in the mediation of apoptosis, transcription of tumor suppressor genes, maintenance of epithelial organization, and control of cell proliferation. Binding of E6 to these proteins cumulatively contributes to the oncogenic potential of HPV. This paper provides an overview of these cellular protein partners of HR-E6, the motifs known to mediate oncoprotein binding, and the agents that have the potential to interfere with E6 expression and activity and thus prevent the subsequent progression to oncogenesis.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Apoptosis
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Cell Adhesion
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Cell Polarity
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Cell Proliferation
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Chromosomal Instability
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Female
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Human papillomavirus 16 / metabolism*
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Human papillomavirus 16 / pathogenicity*
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Humans
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Oncogene Proteins, Viral / chemistry
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Oncogene Proteins, Viral / immunology
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Oncogene Proteins, Viral / metabolism*
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Papillomavirus Infections / immunology
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Papillomavirus Infections / prevention & control
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Papillomavirus Infections / therapy
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Papillomavirus Infections / virology*
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Protein Binding
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Repressor Proteins / chemistry
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Repressor Proteins / immunology
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Repressor Proteins / metabolism*
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Transcription, Genetic
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Tumor Suppressor Protein p53 / metabolism
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Uterine Cervical Neoplasms / prevention & control
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Uterine Cervical Neoplasms / therapy
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Uterine Cervical Neoplasms / virology*
Substances
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E6 protein, Human papillomavirus type 16
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Oncogene Proteins, Viral
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Repressor Proteins
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Tumor Suppressor Protein p53