摘要
简介:埃-巴二氏病毒相关胃癌(EBVaGC)在所有胃癌中占9%,它构成一个独特的临床病理和分子实体。病毒在EBVaGC中表达的模式不能把其定为任何先前的EBV相关的恶性肿瘤。证据支持,病毒在EBVaGC中表达特点是高表达的BamH1 -右向转录(BART),低水平的EBNA-1和缺乏LMP1。该bamh1-a区域高转录活性是重要的定向表达BART miRNAs,在上皮细胞感染和癌变过程中这些miRNA起到了关键作用。一些研究表明,启动子甲基化也是有一个突出的特点。基于最近的TCGA报告,在EBVaGC中基因组改变特定的指纹被PIK3CA,ARID1A和BCOR等突变基因标记,扩增保护JAK2,PD-L1和PD-L2蛋白的9p24. 1基因。病毒基因表达的具体方案,在EBVaGC靶细胞信号通路中发现有病毒基因的表达、基因启动子甲基化、基因组突变,这些都导致细胞增殖,增加细胞的存活,免疫逃逸,增强EMT和干性特征的采集。对于EBV参与慢性胃炎的过程现在了解的很少,但一些研究认为,EBV与幽门螺杆菌相似,早期GC致癌过程是通过促进慢性炎症和增加组织损伤而进行的。 结论:我们讨论了通过EBV在胃上皮中促进的主要和特定的致癌途径。
关键词: 胃癌,埃-巴二氏病毒,BamH1 -右向转录的miRNA,EB 病毒转录的核内小RNA,EB病毒核抗原,EBV潜伏膜蛋白,甲基化表型,慢性炎症。
Current Cancer Drug Targets
Title:Epstein-Barr Virus-associated Gastric Cancer and Potential Mechanisms of Oncogenesis
Volume: 17 Issue: 6
关键词: 胃癌,埃-巴二氏病毒,BamH1 -右向转录的miRNA,EB 病毒转录的核内小RNA,EB病毒核抗原,EBV潜伏膜蛋白,甲基化表型,慢性炎症。
摘要: Introduction: EBV-associated Gastric Cancer (EBVaGC) comprises about 9% of all cases of GC and constitutes a distinct clinicopathological and molecular entity. The pattern of viral expression in EBVaGC cannot be set to any of the previously EBV-associated malignancies. Several lines of evidence support that viral expression in EBVaGC is characterized by high transcription of the BamH1- A rightward transcript (BART), low-levels of EBNA-1 and lack of LMP1. The high transcription activity of the BamH1-A region is importantly directed to express BART miRNAs, supporting a critical role for these miRNAs during epithelial cell infection and carcinogenesis. Several studies have shown that promoter hypermethylation is also a prominent feature of EBVaGC. Based on the recent TCGA report, the specific fingerprint of genomic alterations in EBVaGC is marked by mutations in PIK3CA, ARID1A and BCOR genes, and amplification of 9p24.1 that harbors the genes for the JAK2, PD-L1 and PD-L2 proteins. The specific programs of viral gene expression, promoter methylation and genomic mutations found in EBVaGC target cell signaling pathways leading to increased proliferation, increased cell survival, immune evasion, augmented EMT and acquisition of stemness features. Less understood is the participation of EBV in chronic gastric inflammation, but some studies argue that EBV, similar to and together with Helicobacter pylori, is an early participant in the GC oncogenic process through promoting chronic inflammation and increased tissue damage.
Conclusion: Here, we discuss the principal and distinctive carcinogenic routes promoted by EBV in the gastric epithelium.Export Options
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Cite this article as:
Epstein-Barr Virus-associated Gastric Cancer and Potential Mechanisms of Oncogenesis, Current Cancer Drug Targets 2017; 17 (6) . https://dx.doi.org/10.2174/1568009616666160926124923
DOI https://dx.doi.org/10.2174/1568009616666160926124923 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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