卡波氏肉瘤病毒（KSHV）感染常导致艾滋患者并发艾滋相关的卡波氏肉瘤（AIDS-KS）。AIDS-KS具有异常的血管生成和高度的侵袭转移特征，往往预后差、死亡率高。尽管长链非编码RNA（lncRNAs）能够参与病毒的生命活动与致病过程，然而有关宿主编码的lncRNAs在KSHV诱导KS发生中的作用目前并不清楚。我们最近通过lncRNA芯片检测获得了KSHV感染内皮细胞的lncRNAs差异表达谱；预实验结果发现，部分lncRNAs可能通过与蛋白结合或调控微小RNA的方式参与KSHV诱导内皮细胞迁移侵袭与血管生成。因此，本项目拟（1）鉴定参与调控KSHV诱导内皮细胞迁移侵袭与血管生成的lncRNAs；（2）分别从蛋白互作和竞争性内源性RNA层面阐述上述lncRNAs调控KSHV诱导细胞迁移侵袭与血管生成的分子机制。本研究致力于阐明KSHV的致瘤机制，为探索治疗AIDS-KS的分子靶点奠定基础。

Kaposi’s sarcoma-associated herpesvirus (KSHV) infection frequently leads to occurrence of AIDS-Kaposi’s sarcoma (AIDS-KS) in AIDS patients. With significant mortality and morbidity, AIDS-KS is characterized by excessive deregulation of angiogenesis and extreme invasiveness. The regulatory potential of long non-coding RNAs (lncRNAs) in viral life cycle and pathogenesis have been widely discussed; however, the roles of cellular lncRNAs in the development of KS remain unclear. We have recently discovered the lncRNAs differential expression profile of KSHV-infected endothelial cells by lncRNA microarray, and found that several lncRNAs may participate in KSHV-induced migration, invasion and angiogenesis by interaction with proteins or regulation of microRNAs. Thus, our expectations are to identify specific lncRNAs that are involved in KSHV-induced cell migration, invasion and angiogenesis, and to explore their molecular mechanisms in the terms of protein interaction and competitive endogenous RNA respectively. This project will shed light on the mechanisms of KSHV tumorigenesis and reach a basis for studying potential targets of AIDS-KS clinical therapy.