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Inhibition of HPV-16 E7 oncogenic activity by HPV-16 E2

Oncogene volume 28, pages 2299–2304 (2009)Cite this article

Abstract

Human papillomavirus (HPV) E7 is essential in inducing S-phase progression in differentiating epithelial cells. We have previously shown that HPV-16 E7 activity can be controlled by a direct interaction with the viral transcriptional activator E2, thereby inhibiting transforming potential of E7. We have extended these analyses to show that E2 induces a generalized re-localization of E7 within the cell nucleus, one potential consequence of which is the inhibition of E7-induced degradation of pRb. Most importantly, we show that E2 can also inhibit the ability of E7 to induce centrosome abnormalities, thus preventing aberrant mitoses. Taken together, these studies highlight the central importance of E2 in controlling the functions of E7, independently of the ability of E2 to regulate transcription.

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Acknowledgements

We thank Daniela Gardiol, David Pim and Miranda Thomas for comments on the paper. We also thank Karl Münger for providing anti-HPV-16 E7 monoclonal antibody. This work was supported in part by a research grant from the Associazione Italiana per la Ricerca sul Cancro. EI, DJ and JD were supported by the UK Medical Research Council.

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  1. N Gammoh and E Isaacson: These authors contributed equally to this work.

Authors and Affiliations

  1. International Centre for Genetic Engineering and Biotechnology, Trieste, Italy

    N Gammoh, V Tomaić & L Banks

  2. Division of Virology, MRC National Institute for Medical Research, London, UK

    E Isaacson, D J Jackson & J Doorbar

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  1. N Gammoh
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  2. E Isaacson
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  3. V Tomaić
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  4. D J Jackson
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  5. J Doorbar
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  6. L Banks
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Correspondence to J Doorbar or L Banks.

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Gammoh, N., Isaacson, E., Tomaić, V. et al. Inhibition of HPV-16 E7 oncogenic activity by HPV-16 E2. Oncogene 28, 2299–2304 (2009). https://doi.org/10.1038/onc.2009.78

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