EB病毒ncRNA-EBER1与宿主细胞microRNA-203相互抑制的分子机制

EB病毒（Epstein-barr virus, EBV）在鼻咽癌（nasopharyngeal carcinoma, NPC）发生中发挥病因学作用，但其作用机制尚未明了。我们前期研究发现，在正常鼻咽上皮细胞中EBV非编码RNA1（ncRNA-EBER1）下调抑瘤分子microRNA-203（miR-203）的表达；在鼻咽癌组织中亦发现EBER1与miR-203表达水平成负相关。我们前期实验已证实EBER1是受miR-203调控的靶基因。因此，miR-203能抑制EBER1的表达。本项目拟以前期工作为基础，深入研究EBER1与miR-203相互抑制的分子调控机制。本项目的完成为阐明病毒与宿主细胞相互作用网络提供新的理论依据；为NPC和EBV感染相关疾病提供新的诊治靶标。

Epstein-barr virus（EBV）play a key role in the pathogenesis of nasopharyngeal carcinoma（NPC), but the mechanism is unclear. Our previous study found down-regulation of microRNA-203 (miR-203) by the infection of EBV in normal Epithelial cell and nasopharyngeal carcinoma cell lines. Further study showed the level of ncRNA-EBER1 of EBV was negatively related to the miR-203 in NPC tissues.Thus, EBER1 is also a target gene of miR-203, miR-203 could down-regulate the expression of EBER1. Our research aim to molecular mechanism of mutual inhibition between EB virus noncoding RNA EBER1 and host cell miR-203. Our research could provide new theoretical proof of the interaction between virus and human cell and offer new markers of NPC and EBV related disease for diagnosis and treatment.