The human papillomavirus E7 protein as a transforming and transactivating factor.
The HPV proteins encoded by the early viral genes, including E6 and E7, are thought to subvert the normal regulatory pathways of infected cells to accommodate viral replication. Mechanistically some of this is accomplished by protein-protein interactions between viral proteins and a number of key cellular regulatory proteins that include tumor suppressor gene products. By undermining cellular regulatory pathways the HPV oncogenes cause hyperproliferation and the perturbation of normal cellular differentiation pathways. Although expression of the high-risk HPV-encoded E6 and E7 oncoproteins may be important prerequisites for cellular transformation, it is very likely that additional cellular changes are necessary for carcinogenic progression. The elucidation of the role of the early HPV genes in the initiation and/or maintenance of carcinogenic progression will continue to be a fascinating area of investigation and may reveal new opportunities for antiviral therapy and antitumor intervention.
Münger
K
K
Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, MD 20892.
Phelps
W C
WC
D000595:Amino Acid Sequence; D000818:Animals; D005260:Female; D016161:Genes, Retinoblastoma; D006801:Humans; D008969:Molecular Sequence Data; D009856:Oncogene Proteins, Viral / Q000737:chemistry* / Q000378:metabolism; D027383:Papillomaviridae; D050725:Papillomavirus E7 Proteins; D015533:Transcriptional Activation; D002583:Uterine Cervical Neoplasms / Q000235:genetics
D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; C059731:oncogene protein E7, Human papillomavirus type 16