Cells expressing HPV16 E7 continue cell cycle progression following DNA damage induced p53 activation.
Stabilisation and activation of p53 contributes to the G1 arrest exhibited by many cells in response to DNA damage. One function of p53 is the transcriptional activation of an inhibitor of cyclin dependent kinases; enzymes which phosphorylate and inactivate the growth inhibitory function of the pRB tumour suppressor protein. In this study we show that expression of either of the human papillomavirus encoded E6 and E7 oncoproteins allows cell cycle progression following DNA damage. This suggests that both viral proteins can function in the same pathway; E6 by directly targeting p53 for degradation and E7 through the interaction with pRB, one of the potential downstream effectors of p53.
Ludwig Institute for Cancer Research, St Mary's Hospital Medical School, London, UK.
E S
ES
Hickman
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SM
Picksley
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KH
Vousden
D001943:Breast Neoplasms / Q000235:genetics / Q000473:pathology; D004249:DNA Damage; D005260:Female; D016193:G1 Phase; D005786:Gene Expression Regulation; D016158:Genes, p53 / Q000502:physiology*; D006801:Humans; D009856:Oncogene Proteins, Viral / Q000032:analysis*; D050725:Papillomavirus E7 Proteins; D012097:Repressor Proteins; D014407:Tumor Cells, Cultured
C068651:E6 protein, Human papillomavirus type 16; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D012097:Repressor Proteins; C059731:oncogene protein E7, Human papillomavirus type 16