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Viral oncogenesis and genomic instability: the centr(osom)al connection Volume 23, issue 5, Septembre-Octobre 2019

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Authors
1 Centre international de recherche
en infectiologie, Équipe oncogenèse
rétrovirale, Inserm U1111,
Université Claude-Bernard
Lyon 1, CNRS, UMR5308,
École normale supérieure de Lyon,
Université de Lyon,
46 allée d’Italie, 69007 Lyon, France
2 Centre international de recherche
en infectiologie, Équipe herpèsvirus
oncogènes, Inserm U1111,
Université Claude-Bernard Lyon 1,
CNRS, UMR5308, École normale
supérieure de Lyon, Université de Lyon,
46 allée d’Italie, 69007 Lyon, France
3 Centre international de recherche
en infectiologie, Équipe herpèsvirus
oncogènes, Inserm U1111,
Université Claude-Bernard Lyon 1,
CNRS, UMR5308,
École normale supérieure de Lyon, Université de Lyon,
46 allée d’Italie,
69007 Lyon, France
4 Centre international de recherche sur le cancer,
Groupe biologie des infections et cancer, 150 cours Albert-Thomas,
69008 Lyon,
France
* Correspondance

Currently, more than 10% of human cancers are associated with viral infection. Studies on oncoviruses led to the development of clinical intervention strategies and elucidated fundamental cellular events altered upon cell transformation. Cancer cells exhibit several hallmarks including genomic instability, defined as a high frequency of mutations including gain or loss of chromosomes. The centrosome is an organelle that governs mitotic chromosome segregation and that functions as a signaling platform downstream of the DNA damage response. Here, we review the current literature to highlight how oncoviruses induce genomic instability via the deregulation of the centrosome. Viral interference with the centrosome duplication cycle, leading to centrosome amplification, is illustrated, with a special emphasis on mechanisms shared by several viral families. In addition, we discuss how oncoviruses could alter the signaling functions of the centrosome, and we comment on the bibliographic gaps that could be addressed by future research.

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