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. © 2007 The Author(s).
| Original language | English |
|---|---|
| Pages (from-to) | 397-408 |
| Number of pages | 12 |
| Journal | Archives of Virology |
| Volume | 153 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 2008 |
ASJC Scopus Subject Areas
- Virology
Keywords
- Cell Polarity
- Cell Proliferation
- Humans
- Tumor Suppressor Protein p53/metabolism
- Uterine Cervical Neoplasms/prevention & control
- Cell Adhesion
- Papillomavirus Infections/immunology
- Animals
- Oncogene Proteins, Viral/chemistry
- Human papillomavirus 16/metabolism
- Repressor Proteins/chemistry
- Protein Binding
- Female
- Transcription, Genetic
- Chromosomal Instability
- Apoptosis
Cite this
- APA
- Standard
- Harvard
- Vancouver
- Author
- BIBTEX
- RIS