炎症调控肿瘤干细胞的发生演进，但肿瘤干细胞炎症微环境构建机制不详。前期工作证实，胶质瘤干细胞（GSC）趋化小胶质细胞（MIG）至其周围，激活MIG的STAT3通路，诱导MIG免疫抑制表型，构建GSC免疫微环境。VEGF能够诱导MIG免疫抑制表型，但进一步研究发现，GSC激活MIG还存在“非VEGF依赖途径”，该途径急需进一步阐明。我们发现，GSC中神经降压肽（NTS）表达上调，阻断NTS可抑制GSC诱导的MIG中STAT3通路激活。文献证实，MIG仅表达NTS受体亚型3（SORT），激活该受体可上调MIG促肿瘤炎症介质的产生。我们提出假说：GSC上调表达NTS，激活MIG的SORT及下游STAT3通路，诱导MIG免疫抑制表型，构建GSC炎症微环境。本研究是前期课题的延续和补充，拟揭示NTS/SORT/STAT3信号轴在构建GSC炎症微环境中的作用，为靶向GSC的胶质瘤治疗策略提供新的思路。

It has confirmed that inflammation regulated generation and progression of tumor stem cell, but the mechanism which architects inflammatory niche of tumor stem cell is still unclear. Our previous work found glioma stem cell(GSC) promoted chemotaxis of microglia(MIG), attracted MIG to its surrounding, activated JAK2/STAT3 signal pathway of MIG, induced MIG’s immunosuppressive phenotype and architect inflammatory niche of GSC. VEGF could induced immunosuppressive MIG, however, further researches found GSC could regulate MIG through “VEGF-independent pathway” which needed to explore urgently. We also discovered neurotensin(NTS) was up-regulated apparently in GSC, blockage of NTS could inhibit activation of STAT3 signal pathway in MIG induced by GSC. It has reported that only neurotensin receptor 3 (Sortilin, SORT) expressed in MIG, activation of SORT could promote expression of pro-tumor inflammatory mediators. We hypothesize that GSC up-regulates NTS which activates SORT and its downstream JAK2/STAT3 signal pathway in adjacent MIG, architects the inflammatory niche of GSC. This research programme is the extension and complement of our previous work, we plan to explore the role of NTS/SORT/STAT3 signal axis in the architecture of GSC''s inflammatory niche initiated by microglia and provide a new strategy for GSC-targeting therapy of malignant glioma.