Role of HPV18 E6 in PKB signal transduction pathways

Background The etiological role of Human Papillomavirus (HPV) in cervical cancer development has been clearly demonstrated, it is known that only a minority of cervical lesions infected with high risk HPVs evolve to higher grade lesions or cervical cancer. It is thought that intratype HPV variations may play an important role in differences in viral biological behaviour. It has been recently reported that E6 protein of high risk HPVs degrades proteins such as p53, Bak, Myc and hDlg which are involved in cellular processes such as proliferation, apoptosis and maintenance of cyto-architecture possibly by the PKB pathway. The objective of this study was to determine the differential contribution of E6 from variants of HPV18 in cell proliferation through the Akt/PKB pathway.