期刊
BIOMOLECULES
卷 12, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/biom12010127
关键词
Epstein-Barr Virus; cancer; tumor suppressor genes; epigenetic; post-translational modifications; EBV nuclear antigens; latent membrane proteins
资金
- World Bank African Centres of Excellence grant [ACE02-WACCBIP]
- DELTAS Africa grant [DEL-15-007]
- New Partnership for Africa's Development Planning and Coordinating Agency (NEPAD Agency)
- UK government
- aWACCBIP DELTAS PhD fellowship
- Wellcome Trust [107755/Z/15/Z]
- WACCBIP ACE PhD fellowship
This review summarizes the mechanisms by which Epstein-Barr virus modulates tumor suppressor genes in associated cancers, ultimately promoting malignancies.
Epstein-Barr virus (EBV) is ubiquitous and carried by approximately 90% of the world's adult population. Several mechanisms and pathways have been proposed as to how EBV facilitates the pathogenesis and progression of malignancies, such as Hodgkin's lymphoma, Burkitt's lymphoma, nasopharyngeal carcinoma, and gastric cancers, the majority of which have been linked to viral proteins that are expressed upon infection including latent membrane proteins (LMPs) and Epstein-Barr virus nuclear antigens (EBNAs). EBV expresses microRNAs that facilitate the progression of some cancers. Mostly, EBV induces epigenetic silencing of tumor suppressor genes, degradation of tumor suppressor mRNA transcripts, post-translational modification, and inactivation of tumor suppressor proteins. This review summarizes the mechanisms by which EBV modulates different tumor suppressors at the molecular and cellular levels in associated cancers. Briefly, EBV gene products upregulate DNA methylases to induce epigenetic silencing of tumor suppressor genes via hypermethylation. MicroRNAs expressed by EBV are also involved in the direct targeting of tumor suppressor genes for degradation, and other EBV gene products directly bind to tumor suppressor proteins to inactivate them. All these processes result in downregulation and impaired function of tumor suppressors, ultimately promoting malignances.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据