Vescovo Tiziana, Pagni Benedetta, Piacentini Mauro, Fimia Gian Maria, Antonioli Manuela
National Institute for Infectious Diseases "Lazzaro Spallanzani" - IRCCS, Rome, Italy.
Department of Biology, University of Rome "Tor Vergata," Rome, Italy.
Front Cell Dev Biol. 2020 Feb 28;8:47. doi: 10.3389/fcell.2020.00047. eCollection 2020.
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.
约20%的癌症病例与感染有关。迄今为止,七种人类病毒已被直接证实与癌症发生相关:高危型人乳头瘤病毒(hrHPV)、默克尔细胞多瘤病毒(MCPyV)、乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)、爱泼斯坦-巴尔病毒(EBV)、卡波西肉瘤相关疱疹病毒(KSHV)以及人类嗜T淋巴细胞病毒1型(HTLV-1)。这些病毒影响宿主细胞中的多种分子机制,常导致慢性炎症、增殖失控和细胞死亡抑制,这些机制虽有利于病毒生命周期,但可能间接促进肿瘤发生。最近,致癌病毒改变自噬的能力正成为人类癌症发生的关键事件,自噬是在对感染的固有免疫反应中激活的一种分解代谢过程。在此,我们总结了目前对人类致癌病毒调节自噬的分子机制以及这种负调节如何影响癌症发展的理解。最后,我们强调了用于治疗病毒相关癌症的新型自噬相关候选药物。