Carcinogenesis Advance Access originally published online on March 7, 2007
Carcinogenesis 2007 28(6):1140-1144; doi:10.1093/carcin/bgm048
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Control of virus infection by tumour suppressors
1 Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza Ramón y Cajal s/n, Madrid 28040, Spain
2 Departamento de Biologia Molecular y Celular, Centro Nacional de Biotecnología, CSIC, Campus Universidad Autónoma de Madrid, Madrid 28049, Spain
3 Molecular Oncology Program, Spanish National Cancer Centre (CNIO), 3 Melchor Fernández Almagro, Madrid 28029, Spain
4 Department of Oncological Sciences, Mount Sinai School of Medicine, One Gustave L, Levy Place, Box 1130, NY 10029, USA
* To whom correspondence should be addressed. Tel: +34 913941746; Fax: +34 913941745;Email: mdcrivas{at}farm.ucm.es
An increasing number of tumour suppressor genes are induced by interferons (IFNs) and may play an important role in the control of cell proliferation induced by this cytokine. In addition, pathways triggered by both tumour suppressors and IFN converge as common targets for non-related tumour viruses. The inhibition of the IFN response by animal viruses is explained by the fundamental role that IFN plays to control virus infection. However, the reasons why many viruses, including those that do not require the replication of the host, target tumour suppressor pathways are varied and are still under investigation. Here we review those findings that support that tumour suppressors may have a role in the control of virus infection.
Abbreviations: ARF, alternative reading frame; IFN, interferon; PKR, dsRNA-dependent protein kinase; PLSCR1, phospholipid scramblase 1; PML, promyelocytic leukaemia; VSV, vesicular stomatitis virus
Received November 30, 2006; revised February 12, 2007; accepted February 26, 2007.
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