Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer

被引:18
作者
Alibek, Kenneth [1 ,2 ]
Irving, Stephanie [1 ]
Sautbayeva, Zarina [1 ]
Kakpenova, Ainur [1 ]
Bekmurzayeva, Aliya [1 ]
Baiken, Yeldar [1 ]
Imangali, Nurgul [3 ]
Shaimerdenova, Madina [3 ]
Mektepbayeva, Damel [1 ]
Balabiyev, Arnat [1 ]
Chinybayeva, Aizada [1 ]
机构
[1] Nazarbayev Univ, Nazarbayev Univ Res & Innovat Syst NURIS, Astana 010000, Kazakhstan
[2] Natl Med Holding, Astana 010000, Kazakhstan
[3] Nazarbayev Univ, Sch Sci & Technol, Astana 010000, Kazakhstan
关键词
Bcl-2; Bcl-xL; Herpesviruses; Human T-lymphotropic virus 1; Human papillomavirus; Hepatitis C virus; Apoptosis; Signaling pathways; Tumor suppressor genes; Cancer; EPSTEIN-BARR-VIRUS; SARCOMA-ASSOCIATED HERPESVIRUS; HUMAN-PAPILLOMAVIRUS TYPE-16; PROTEASOME-MEDIATED DEGRADATION; PRIMARY EFFUSION LYMPHOMA; GROWTH-FACTOR RECEPTOR; I TAX PROTEIN; KAPOSIS-SARCOMA; INHIBITS APOPTOSIS; HTLV-I;
D O I
10.1186/1750-9378-9-44
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
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.
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页数:13
相关论文
共 142 条
[31]   Glioma-Associated Cytomegalovirus Mediates Subversion of the Monocyte Lineage to a Tumor Propagating Phenotype [J].
Dziurzynski, Kristine ;
Wei, Jun ;
Qiao, Wei ;
Hatiboglu, Mustafa Aziz ;
Kong, Ling-Yuan ;
Wu, Adam ;
Wang, Yongtao ;
Cahill, Daniel ;
Levine, Nicholas ;
Prabhu, Sujit ;
Rao, Ganesh ;
Sawaya, Raymond ;
Heimberger, Amy B. .
CLINICAL CANCER RESEARCH, 2011, 17 (14) :4642-4649
[32]   Dysregulation of apoptosis in hepatocellular carcinoma cells [J].
Fabregat, Isabel .
WORLD JOURNAL OF GASTROENTEROLOGY, 2009, 15 (05) :513-520
[33]  
Fedorova N E, 2010, Tsitologiia, V52, P168
[34]   Hepatitis C virus infection and apoptosis [J].
Fischer, Richard ;
Baumert, Thomas ;
Blum, Hubert E. .
WORLD JOURNAL OF GASTROENTEROLOGY, 2007, 13 (36) :4865-4872
[35]   BH3 domains define selective inhibitory interactions with BHRF-1 and KSHVBCL-2 [J].
Flanagan, A. M. ;
Letai, A. .
CELL DEATH AND DIFFERENTIATION, 2008, 15 (03) :580-588
[36]   Epstein-Barr virus interactions with the Bcl-2 protein family and apoptosis in human tumor cells [J].
Fu, Qin ;
He, Chen ;
Mao, Zheng-rong .
JOURNAL OF ZHEJIANG UNIVERSITY-SCIENCE B, 2013, 14 (01) :8-24
[37]   Inhibition of CDK activity and PCNA-dependent DNA replication by p21 is blocked by interaction with the HPV-16 E7 oncoprotein [J].
Funk, JO ;
Waga, S ;
Harry, JB ;
Espling, E ;
Stillman, B ;
Galloway, DA .
GENES & DEVELOPMENT, 1997, 11 (16) :2090-2100
[38]   Interactions between viral nonstructural proteins and host protein hVAP-33 mediate the formation of hepatitis C virus RNA replication complex on lipid raft [J].
Gao, L ;
Aizaki, H ;
He, JW ;
Lai, MMC .
JOURNAL OF VIROLOGY, 2004, 78 (07) :3480-3488
[39]   Cellular transformation by the HTLV-I tax protein, a jack-of-all-trades [J].
Gatza, ML ;
Watt, JC ;
Marriott, SJ .
ONCOGENE, 2003, 22 (33) :5141-5149
[40]   Inhibiting primary effusion lymphoma, by lentiviral vectors encoding short hairpin RNA [J].
Godfrey, A ;
Anderson, J ;
Papanastasiou, A ;
Takeuchi, Y ;
Boshoff, C .
BLOOD, 2005, 105 (06) :2510-2518