Expression of HPV16 E5 produces enlarged nuclei and polyploidy through endoreplication
- Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK (United States)
- Cell Cycle and Cancer Biology, Oklahoma Medical Research Foundation, Oklahoma City, OK (United States)
- Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK (United States)
- Nebraska Center for Virology, University of Nebraska, Lincoln, NE (United States)
Anogenital cancers and head and neck cancers are causally associated with infection by high-risk human papillomavirus (HPV). The mechanism by which high-risk HPVs contribute to oncogenesis is poorly understood. HPV16 encodes three genes (HPV16 E5, E6, and E7) that can transform cells when expressed independently. HPV16 E6 and E7 have well-described roles causing genomic instability and unregulated cell cycle progression. The role of HPV16 E5 in cell transformation remains to be elucidated. Expression of HPV16 E5 results in enlarged, polyploid nuclei that are dependent on the level and duration of HPV16 E5 expression. Live cell imaging data indicate that these changes do not arise from cell-cell fusion or failed cytokinesis. The increase in nuclear size is a continual process that requires DNA synthesis. We conclude that HPV16 E5 produces polyploid cells by endoreplication. These findings provide insight into how HPV16 E5 can contribute to cell transformation.
- OSTI ID:
- 21460273
- Journal Information:
- Virology, Vol. 405, Issue 2; Other Information: DOI: 10.1016/j.virol.2010.06.025; PII: S0042-6822(10)00407-1; Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; ISSN 0042-6822
- Country of Publication:
- United States
- Language:
- English
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