期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 8, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2020.00047
关键词
oncogenic (or carcinogenic) viruses; autopaghy; human papillomavirus (HPV); Merkel cell polyomavirus (MCPyV); hepatitis B and C viruses (HBV and HCV); Epstein-Barr virus (EBV); Kaposi's sarcoma-associated herpesvirus (KSHV); human T-lymphotropic virus 1 (HTLV-1)
资金
- Fondazione Umberto Veronesi
- FRIAS COFUND Fellowship Programme (University of Freiburg, Germany) [609305]
- People Programme (Marie Curie Actions) of the European Union's 7th Framework Programme (FP/2007-2013) under REA grant [609305]
- Transautophagy COST action [CA15138]
- Italian Ministry of Health [GR-2013-02359524]
- AIRC [17404, 21880]
- Russian Government Programme for the Recruitment of the Leading Scientists into the Russian Institutions of Higher Education [14.W03.31.0029]
About 20% of total cancer cases are associated to infections. To date, seven human viruses have been directly linked to cancer development: high-risk human papillomaviruses (hrHPVs), Merkel cell polyomavirus (MCPyV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human T-lymphotropic virus 1 (HTLV-1). These viruses impact on several molecular mechanisms in the host cells, often resulting in chronic inflammation, uncontrolled proliferation, and cell death inhibition, and mechanisms, which favor viral life cycle but may indirectly promote tumorigenesis. Recently, the ability of oncogenic viruses to alter autophagy, a catabolic process activated during the innate immune response to infections, is emerging as a key event for the onset of human cancers. Here, we summarize the current understanding of the molecular mechanisms by which human oncogenic viruses regulate autophagy and how this negative regulation impacts on cancer development. Finally, we highlight novel autophagy-related candidates for the treatment of virus-related cancers.
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