Liu Yitong, Hu Zhizhong, Zhang Yang, Wang Chengkun
Hunan Province Key Laboratory of Tumor Cellular & Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, 28 West Changsheng Road, Hengyang, 421001, Hunan, People's Republic of China.
Cancer Cell Int. 2021 May 25;21(1):278. doi: 10.1186/s12935-021-01986-w.
Epstein Barr-virus (EBV) is related to several cancers. Long non-coding RNAs (lncRNAs) act by regulating target genes and are involved in tumourigenesis. However, the role of lncRNAs in EBV-associated cancers is rarely reported. Understanding the role and mechanism of lncRNAs in EBV-associated cancers may contribute to diagnosis, prognosis and clinical therapy in the future. EBV encodes not only miRNAs, but also BART lncRNAs during latency and the BHLF1 lncRNA during both the latent and lytic phases. These lncRNAs can be targeted regulate inflammation, invasion, and migration and thus tumourigenesis. The products of EBV also directly and indirectly regulate host lncRNAs, including LINC00312, NORAD CYTOR, SHNG8, SHNG5, MINCR, lncRNA-BC200, LINC00672, MALATI1, LINC00982, LINC02067, IGFBP7-AS1, LOC100505716, LOC100128494, NAG7 and RP4-794H19.1, to facilitate tumourigenesis using different mechanisms. Additionally, lncRNAs have been previously validated to interact with microRNAs (miRNAs), and lncRNAs and miRNAs mutually suppress each other. The EBV-miR-BART6-3p/LOC553103/STMN1 axis inhibits EBV-associated tumour cell proliferation. Additionally, H. pylori-EBV co-infection promotes inflammatory lesions and results in EMT. HPV-EBV co-infection inhibits the transition from latency to lytic replication. KSHV-EBV co-infection aggravates tumourigenesis in huNSG mice. COVID-19-EBV co-infection may activate the immune system to destroy a tumour, although this situation is rare and the mechanism requires further confirmation. Hopefully, this information will shed some light on tumour therapy strategies tumourigenesis. Additionally, this strategy benefits for infected patients by preventing latency to lytic replication. Understanding the role and expression of lnRNAs in these two phases of EBV is critical to control the transition from latency to the lytic replication phase. This review presents differential expressed lncRNAs in EBV-associated cancers and provides resources to aid in developing superior strategies for clinical therapy.
爱泼斯坦-巴尔病毒(EBV)与多种癌症相关。长链非编码RNA(lncRNAs)通过调控靶基因发挥作用,并参与肿瘤发生。然而,lncRNAs在EBV相关癌症中的作用鲜有报道。了解lncRNAs在EBV相关癌症中的作用和机制可能有助于未来的诊断、预后评估及临床治疗。EBV在潜伏期间不仅编码miRNAs,还编码BART lncRNAs,在潜伏和裂解阶段均编码BHLF1 lncRNA。这些lncRNAs可靶向调控炎症、侵袭和迁移,进而影响肿瘤发生。EBV的产物还直接或间接调控宿主lncRNAs,包括LINC00312、NORAD CYTOR、SHNG8、SHNG5、MINCR、lncRNA-BC200、LINC00672、MALATI1、LINC00982、LINC02067、IGFBP7-AS1、LOC100505716、LOC100128494、NAG7和RP4-794H19.1,通过不同机制促进肿瘤发生。此外,lncRNAs此前已被证实可与微小RNA(miRNAs)相互作用,lncRNAs和miRNAs相互抑制。EBV-miR-BART6-3p/LOC553103/STMN1轴抑制EBV相关肿瘤细胞增殖。此外,幽门螺杆菌-EBV共感染促进炎症病变并导致上皮-间质转化。人乳头瘤病毒-EBV共感染抑制从潜伏到裂解复制的转变。卡波西肉瘤相关疱疹病毒-EBV共感染加剧人源化NSG小鼠的肿瘤发生。新冠病毒-EBV共感染可能激活免疫系统以破坏肿瘤,尽管这种情况罕见且机制需进一步证实。希望这些信息能为肿瘤治疗策略提供一些启示。此外,该策略通过防止从潜伏到裂解复制,使感染患者受益。了解lnRNAs在EBV这两个阶段的作用和表达对于控制从潜伏到裂解复制阶段的转变至关重要。本综述介绍了EBV相关癌症中差异表达的lncRNAs,并提供资源以帮助制定更优的临床治疗策略。