Publication | Open Access
Tumor suppressor or oncogene? A critical role of the human papillomavirus (HPV) E2 protein in cervical cancer progression.
54
Citations
132
References
2011
Year
Viral ReplicationCervical Cancer ProgressionHpv-induced CarcinogenesisPathologyMolecular BiologyCancer BiologyTumor BiologyCancer-associated VirusTranscriptional RegulationHost Cell CycleHuman Papillomavirus VaccinesPublic HealthVirus GeneOncogenic AgentGene ExpressionCell BiologyE2 ProteinCervical CancerHpv E2Tumor SuppressorSystems BiologyMedicineViral OncologyPrecancerous Lesions
The papillomavirus (PV) E2 proteins have been shown to exert many functions in the viral cycle including pivotal roles in transcriptional regulation and in viral DNA replication. Besides these historical roles, which rely on their aptitude to bind to specific DNA sequences, E2 has also been shown to modulate the host cells through direct protein interactions mainly through its amino terminal transactivation domain. We will describe here some of these new functions of E2 and their potential implication in the HPV-induced carcinogenesis. More particularly we will focus on E2-mediated modulation of the host cell cycle and consequences to cell transformation. In all, the HPV E2 proteins exhibit complex functions independent of transcription that can modulate the host cells in concert with the viral vegetative cycle and which could be involved in early carcinogenesis.
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