卡波氏肉瘤病毒（KSHV）感染导致艾滋患者中卡波氏肉瘤（AIDS-KS）频繁发生。KSHV病毒白介素6（vIL-6）通过调控JAK/STAT通路诱导血管生成，但参与此过程的下游靶蛋白并不清楚。课题组前期研究发现，艾滋病毒编码的相关蛋白能够协同KSHV vIL-6诱导血管生成（Oncogene，2013）。我们最近又通过iTRAQ技术获得了vIL-6诱导内皮细胞血管生成中的蛋白质组学差异表达谱。那么vIL-6通过调控JAK/STAT通路下游哪些关键蛋白诱导血管生成？. 本研究拟（1）证实vIL-6能够诱导内皮细胞血管生成；（2）鉴定此过程中的蛋白质组学差异表达谱及关键蛋白；（3）通过研究关键蛋白及其下游基因与JAK/STAT通路的关系，阐述vIL-6诱导血管生成的分子机制。. 本研究的结果将有助于阐明AIDS-KS致瘤机制，为AIDS-KS的治疗提供潜在的分子靶点。

AIDS-related Kaposi’s sarcoma (AIDS-KS), led by Kaposi’s sarcoma-associated herpesvirus (KSHV) infection, is the most common cancer associated with HIV/AIDS patients. As one of the KSHV-encoded oncoproteins, the molecular mechanisms of viral interleukin-6 (vIL-6)-induced angiogenesis and oncogenesis remains unclear. Our laboratory has recently discovered that HIV-1 Tat and Nef promotes KSHV vIL-6-induced angiogenesis and tumorigenesis by regulating PI3K/AKT signaling pathway both in vitro and in vivo (Oncogene, 2013). By isobaric tags for relative and absolute quantification (iTRAQ), we have also obtained the comparative quantitative proteomics analysis of KSHV vIL-6-induced angiogenesis. However, the critical proteins of JAK/STAT pathway involved in KSHV vIL-6-induced angiogenesis are unknown.. Our expectations are to confirm that KSHV vIL-6 can induce angiogenesis in endothelial cells, to identify the comprehensive proteomics and critical proteins participated in vIL-6-induced angiogenesis, and to elaborate the correlated molecular mechanisms of the critical proteins in this progress.. Our research will contribute to investigate the molecular mechanism of the onset of AIDS-KS, which may provide some effective potential target for the prevention and treatment of AIDS-KS at the molecular level.