
Human Papillomavirus type 77 is a skin type found in non-melanoma skin cancers of immuno-compromised individuals. Although, the HPV77 E6 oncoprotein has been well studied, nothing is known about E7. Studies on mucosal HPV types (e.g. HPV16) showed that E7 deregulates the cell cycle by binding to and promoting degradation of retinoblastoma protein (pRb). Here, we characterized the impact of HPV77 E7 on the cell cycle. We observed that HPV77 E7 associated with pRb with a lower affinity than HPV16 E7, promoting weakly its degradation. Although, HPV16 E7 led to cellular proliferation and accumulation of the cell cycle inhibitor p16(INK4a), both events were not clearly observed in HPV77 E7 cells. Together, these data indicate that HPV77 E7 does not efficiently deregulate the cell cycle, in contrast to several E7s of mucosal HPV types.
Reverse Transcriptase Polymerase Chain Reaction, Papillomavirus E7 Proteins, Cell Cycle, Genetic Vectors, Immunoblotting, Gene Expression, Oncogene Proteins, Viral, Transfection, Retinoblastoma Protein, Mice, NIH 3T3 Cells, Animals, Humans, Cells, Cultured, Cyclin-Dependent Kinase Inhibitor p16, Protein Binding
Reverse Transcriptase Polymerase Chain Reaction, Papillomavirus E7 Proteins, Cell Cycle, Genetic Vectors, Immunoblotting, Gene Expression, Oncogene Proteins, Viral, Transfection, Retinoblastoma Protein, Mice, NIH 3T3 Cells, Animals, Humans, Cells, Cultured, Cyclin-Dependent Kinase Inhibitor p16, Protein Binding
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