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Published on: September 20, 2019
[Viral oncogenesis and genomic instability: the centr(osom)al connection]
Élodie Teruel1, Henri Gruffat2, Massimo Tommasino3
1Centre 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, 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.
None:
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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