胶质瘤是一种典型的血管依赖性恶性肿瘤，它的发生发展必须依赖大量新的血管生成。近年来诸多证据表明miRNA在胶质瘤发生发展中发挥重要作用。我们前期实验结果提示与正常脑组织相比，胶质瘤组织中miR-26a呈高表达，而miR-143呈低表达；下调miR-26a可抑制胶质瘤细胞增殖和微管形成并引起miR-143升高；两者可能通过p53存在相互作用。据此我们提出假说：miR-26a通过p53调控miR-143的表达，三者相互作用调控胶质瘤形成和新的血管生成。本课题拟建立miR-26a/p53/miR-143不同表达状态细胞模型并结合靶基因验证和转录调控研究，深入探讨miR-26a和miR-143之间的相互调控关系及其在胶质瘤形成和新的血管生成中的作用机制，揭示"miRNA-miRNA调控"的新机制，为现有的神经胶质瘤发生发展机制提供理论依据，为建立微小RNA靶向治疗技术提供新的思路。

Glioma is a kind of typical vascular dependence malignant tumor, whose initation and development greatly rely on angiogenesis. MicroRNAs control the initation and development of glioma through networked cascade, feedback and synergy effect. Our preliminary data showed the following results: i).compared to the normal brain tissues, the expression levels of miR-26a were up-regulated and the expression levels of miR-143 were down-regulated in glioma tissues; ii). inhibition of miR-26a or overexpression of miR-143 markedly reduced glioma cells proliferation and tube formation；ⅲ). inhibition of miR-26a induced miR-143 expression by p53，but the underlying mechanisms are far less known. We hypothesize that miR-26a regulates miR-143 expression via p53, and thus mediating glioma growth and angiogenesis by regulating biological targets of miR-143 and downstream signalings. In this study, we will establish glioma cells stable over/down-expressing miR-26a or p53 or miR-143 as cell models, and conduct gain-of-function experiment, combined with target gene validation and transcription regulation research, further analyzed the mutual regulation relationship between miR-26a and miR-143. This study will reveal miRNA-miRNA regulation, outline the miR-26a/p53/miR-143 model in miRNA regulation network, provide supplementary for glioma initation and development，and establish miRNA based clinical therapy for glioma.