Infectious Agents and Cancer | |
Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer | |
Aizada Chinybayeva1  Arnat Balabiyev1  Damel Mektepbayeva1  Madina Shaimerdenova3  Nurgul Imangali3  Yeldar Baiken1  Aliya Bekmurzayeva1  Ainur Kakpenova1  Zarina Sautbayeva1  Stephanie Irving1  Kenneth Alibek2  | |
[1] Nazarbayev University Research and Innovation System (NURIS), Nazarbayev University, 53 Kabanbay Batyr Avenue, Astana 010000, Kazakhstan;National Medical Holding, 2 Syganak Street, Astana 010000, Kazakhstan;School of Science and Technology, Nazarbayev University, 53 Kabanbay Batyr Avenue, Astana 010000, Kazakhstan | |
关键词: Cancer; Tumor suppressor genes; Signaling pathways; Apoptosis; Hepatitis C virus; Human papillomavirus; Human T-lymphotropic virus 1; Herpesviruses; Bcl-xL; Bcl-2; | |
Others : 1133750 DOI : 10.1186/1750-9378-9-44 |
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received in 2014-09-23, accepted in 2014-11-25, 发布年份 2014 |
【 摘 要 】
The Bcl proteins play a critical role in apoptosis, as mutations in family members interfere with normal programmed cell death. Such events can cause cell transformation, potentially leading to cancer. Recent discoveries indicate that some viral proteins interfere with Bcl proteins either directly or indirectly; however, these data have not been systematically described. Some viruses encode proteins that reprogramme host cellular signalling pathways controlling cell differentiation, proliferation, genomic integrity, cell death, and immune system recognition. This review analyses and summarises the existing data and discusses how viral proteins interfere with normal pro- and anti-apoptotic functions of Bcl-2 and Bcl-xL. Particularly, this article focuses on how viral proteins, such as Herpesviruses, HTLV-1, HPV and HCV, block apoptosis and how accumulation of such interference predisposes cancer development. Finally, we discuss possible ways to prevent and treat cancers using a combination of traditional therapies and antiviral preparations that are effective against these viruses.
【 授权许可】
2014 Alibek et al.; licensee BioMed Central.
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