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Human papillomavirus E7 oncoprotein targets RNF168 to hijack the host DNA damage response
Abstract
Significance: Human papillomaviruses (HPVs) cause 5% of all cancers, including cervical cancers and a growing number of oropharyngeal cancers, which are reaching epidemic proportion. While HPV oncogenes promote the acquisition of cancer hallmarks such as sustained proliferation and resistance to cell death by targeting the p53 and pRb pathways, the mechanism by which they induce genomic instability leading to cellular transformation remains largely unknown. This paper describes how the HPV oncoprotein E7 directly impedes the cellular response to DNA double-strand breaks by interacting with a previously uncharacterized domain of the E3 ubiquitin ligase RNF168. As the function of RNF168 is essential for proper DNA repair, our findings reveal a mechanism by which HPV induces genomic instability and fuels cancer progression.
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“HPV E7 has been shown to hijack the E3 ubiquitin ligase RNF168, which is critical to proper DSB repair, in order to promote the viral replication cycle. This interaction perturbs cellular DSB signalling, leading to disruption of host chromatin response to DNA breaks and promoting genomic instability that drives oncogenesis [321]”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [321]
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A review of human carcinogens—Part B: biological agents
Bouvard, V., Baan, R., Straif, K., Grosse, Y., Secretan, B., Ghissassi, F. E., Benbrahim-Tallaa, L., Guha, N., Freeman, C., Galichet, L., et al. (2009) · The Lancet Oncology · doi:10.1016/s1470-2045(09)70096-8 · Cited by 2,935
Easy quantitative assessment of genome editing by sequence trace decomposition
Brinkman, E. K., Chen, T., Amendola, M., & van Steensel, B. (2014) · Nucleic Acids Research · doi:10.1093/nar/gku936 · Cited by 2,390
Kiyono, T., Foster, S. A., Koop, J. I., McDougall, J. K., Galloway, D. A., & Klingelhutz, A. J. (1998) · Nature · doi:10.1038/23962 · Cited by 1,206
The control of DNA repair by the cell cycle
Hustedt, N., & Durocher, D. (2017) · Nature Cell Biology · doi:10.1038/ncb3452 · Cited by 738
53BP1 is a reader of the DNA-damage-induced H2A Lys 15 ubiquitin mark
Fradet-Turcotte, A., Canny, M. D., Escribano-Díaz, C., Orthwein, A., Leung, C. C. Y., Huang, H., Landry, M.-C., Kitevski-LeBlanc, J., Noordermeer, S. M., Sicheri, F., et al. (2013) · Nature · doi:10.1038/nature12318 · Cited by 686
Self-citationAcetylation limits 53BP1 association with damaged chromatin to promote homologous recombination
Tang, J., Cho, N. W., Cui, G., Manion, E. M., Shanbhag, N. M., Botuyan, M. V., Mer, G., & Greenberg, R. A. (2013) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.2499 · Cited by 521
Activation of the Cellular DNA Damage Response in the Absence of DNA Lesions
Soutoglou, E., & Misteli, T. (2008) · Science · doi:10.1126/science.1159051 · Cited by 299
White, E. A., Sowa, M. E., Tan, M. J. A., Jeudy, S., Hayes, S. D., Santha, S., Münger, K., Harper, J. W., & Howley, P. M. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1116776109 · Cited by 198
Panier, S., Ichijima, Y., Fradet-Turcotte, A., Leung, C. C. Y., Kaustov, L., Arrowsmith, C. H., & Durocher, D. (2012) · Molecular Cell · doi:10.1016/j.molcel.2012.05.045 · Cited by 152
Self-citation
Research works printed but not linked: 67
- 10.1016/S1470-2045(12)70137-7 · DOI
- 10.1016/j.chom.2014.02.011 · DOI
- 10.1016/j.virol.2004.03.033 · DOI
- 10.1002/rmv.1822 · DOI
- 10.1200/JCO.2015.61.6995 · DOI
- 10.3747/co.20.1375 · DOI
- 10.1515/hsz-2017-0113 · DOI · Paper page
- 10.3390/v7052450 · DOI
- 10.1146/annurev-virology-092917-043534 · DOI
- 10.1128/JVI.00247-12 · DOI
- 10.1371/journal.ppat.1000605 · DOI · Paper page
- 10.1371/journal.ppat.1003777 · DOI
- 10.1371/journal.ppat.1000397 · DOI · Paper page
- 10.1128/JVI.00517-14 · DOI
- 10.1128/JVI.02495-15 · DOI
- 10.1128/mBio.00064-18 · DOI
- 10.1016/j.cell.2011.02.013 · DOI · Paper page
- 10.1016/0092-8674(93)90493-A · DOI
- 10.15252/embj.201592595 · DOI
- 10.1098/rstb.2016.0280 · DOI
- 10.1016/j.cell.2012.08.005 · DOI
- 10.7554/eLife.23872 · DOI
- 10.1016/j.molcel.2017.04.009 · DOI
- 10.1038/nature18951 · DOI
- 10.15252/embr.201847560 · DOI
- 10.1371/journal.pgen.1001381 · DOI
- 10.1016/j.cell.2008.12.042 · DOI
- 10.1016/j.cell.2012.06.039 · DOI
- 10.1158/2159-8290.CD-12-0095 · DOI · Paper page
- 10.1126/scisignal.2004088 · DOI · Paper page
- 10.1093/emboj/17.6.1768 · DOI
- 10.1038/ncb2201 · DOI
- 10.1083/jcb.201011083 · DOI
- 10.1038/s41556-019-0293-6 · DOI
- 10.1128/JVI.01002-12 · DOI
- 10.1016/j.molcel.2010.05.020 · DOI · Paper page
- 10.1038/onc.2015.268 · DOI
- 10.1128/JVI.78.7.3533-3541.2004 · DOI
- 10.1038/sj.emboj.7600651 · DOI · Paper page
- 10.1016/j.virol.2013.04.013 · DOI
- 10.1128/JVI.00643-11 · DOI · Paper page
- 10.1186/s12985-018-1086-4 · DOI
- 10.1016/j.molcel.2018.07.011 · DOI
- 10.1073/pnas.212519499 · DOI
- 10.1016/j.molcel.2018.12.010 · DOI
- 10.7554/eLife.20922 · DOI
- 10.1016/j.coviro.2018.08.017 · DOI
- 10.1038/emboj.2009.400 · DOI
- 10.1371/journal.ppat.1002084 · DOI
- 10.1016/j.molcel.2012.02.004 · DOI
- 10.1016/j.virol.2019.03.001 · DOI
- 10.1371/journal.pgen.1004178 · DOI
- 10.1128/JVI.00262-18 · DOI
- 10.1093/nar/gkt729 · DOI
- 10.1101/gad.1735109 · DOI
- 10.1038/ncb2017 · DOI · Paper page
- 10.1038/nrc2886 · DOI
- 10.1038/emboj.2012.47 · DOI
- 10.1128/JVI.01318-17 · DOI
- 10.1128/JVI.00881-07 · DOI · Paper page
- 10.1128/JVI.01012-17 · DOI
- 10.1093/nar/gkv336 · DOI
- 10.1016/j.cell.2017.08.001 · DOI
- R. Wilson, L. A. Laimins, Differentiation of HPV-containing cells using organotypic “raft” culture or methylcellulose. Methods Mol. Med. 119, 157–169 (2005).
- 10.1128/JVI.77.5.2819-2831.2003 · DOI
- 10.1093/nar/gkv993 · DOI
- 10.3390/v9090252 · DOI
Cited by
Basukala, O., & Banks, L. (2021) · Viruses · doi:10.3390/v13101892 · Cited by 137
Metadata
- Authors
- Sitz, J., Blanchet, S. A., Gameiro, S. F., Biquand, E., Morgan, T. M., Galloy, M., Dessapt, J., Lavoie, E. G., Blondeau, A., Smith, B. C., Mymryk, J. S., Moody, C. A., & Fradet-Turcotte, A.
- Affiliations
- Oncology Division, Centre Hospitalier Universitaire (CHU) de Québec-Université Laval Research Center, Québec, QC, Canada G1R 1S3;
- Department of Microbiology & Immunology, The University of Western Ontario, London, ON, Canada N6A 3K7;
- Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;
- Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2019-09-09
- Volume
- 116
- Issue
- 39
- Pages
- 19552-19562
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 77
- References
- 9
- Language
- en
- Funders
- Gouvernement du Canada | CIHR | Institute of Cancer Research (152948)
- Gouvernement du Canada | CIHR | Institute of Infection and Immunity (142491)
- Cancer Research Society (19590)
- HHS | NIH | National Cancer Institute (CA181581, CA226523)
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- Sitz, J., Blanchet, S. A., Gameiro, S. F., Biquand, E., Morgan, T. M., Galloy, M., Dessapt, J., Lavoie, E. G., Blondeau, A., Smith, B. C., Mymryk, J. S., Moody, C. A., & Fradet-Turcotte, A. (2019). Human papillomavirus E7 oncoprotein targets RNF168 to hijack the host DNA damage response. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1906102116