Understanding the mechanisms of HPV-related carcinogenesis: Implications for cell cycle dynamics.

ABSTRACT: The role of human papillomavirus (HPV) as a causative agent for epithelial cancers is well-known, but many open questions remain regarding the downstream gene regulatory effects of viral proteins E6 and E7 on the cell cycle. Here, we extend a cell cycle model originally presented by Gérard and Goldbeter (2009) in order to capture the effects of E6 and E7 on key actors in the cell cycle. Results suggest that E6 is sufficient to reverse p53-induced quiescence, while E7 is sufficient to reverse p16^INK4a-induced quiescence; both E6 and E7 are necessary when p53 and p16^INK4a are both active. Moreover, E7 appears to play a role as a "growth factor substitute", inducing cell division in the absence of growth factor. Low levels of E7 may permit regular cell division, but the

SUBMITTER: Sund DT 

PROVIDER: S-EPMC9838640 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature