胶质瘤新血管的形成是其恶性程度的重要标志之一。胶质瘤通过血管生成与血管拟态的双重血液供应，使得传统的抗肿瘤血管治疗无法彻底阻断胶质瘤的血供，影响其治疗与预后。我们通过前期研究发现，外泌体RPL34-AS1在胶质瘤患者血清中显著增高，具有促进胶质瘤血管生成的能力。本项目拟从大样本胶质瘤血清检测作为切入点，判定外泌体RPL34-AS1作为胶质瘤临床诊断和预后标记物的可行性，进而发掘其来源，深入探究其在内皮细胞中促进血管向肿瘤内生成及在胶质瘤干细胞中诱导血管拟态生成的作用。为进一步探讨其作用机制，我们将继续阐明其与VEGFR-2的结合关系，从而揭示其促进肿瘤血管生成的原因。最后通过靶向抑制RPL34-AS1，有效减少胶质瘤血管生成，显著延长生存期。本研究为进一步认识胶质瘤的血管生成机制提供了全新的视角和理论基础，并为胶质瘤的诊断及预后判断提供了新的靶点，为胶质瘤的治疗提供的新的思路。

Glioma neovascularization is one of the important indicators of malignancy. Traditional antineoplastic treatment cannot obstruct blood supply of glioma completely on account of the dual formation modes of angiogenesis and vasculogenic mimicry, which affect treatment and prognosis. Exosomes play an important role through the transformation of the tumor microenvironment during this process. We have found there is a significant increase of RPL34-AS1 in exosomes in serum of glioma patients promoting glioma neovascularization. This project intends to start with assessment of exosome RPL34-AS1 in a large number of glioma serum samples to determine its feasibility being a clinical diagnosis and prognostic marker of glioma, following with confirming the source of it. We will explore its promotion of blood vessels in endothelial cells and induction of vascular mimicry in glioma stem cells in further study. To move forward, we will elucidate its mechanism binding with VEGFR-2 to reveal its cause of tumor neovascularization. Finally, glioma is effectively reduced through targeting inhibition of RPL34-AS1, meanwhile survival is significantly prolonged. This study provides a new perspective and theoretical basis for further understanding of mechanism of glioma neovascularization, providing a new target for diagnosis and prognosis of glioma and a new idea for treatment of glioma.