胶质瘤严重威胁人类健康，其病情进展受到众多胞内信号通路调控，其中ERK和NF-κB通路是调控肿瘤增殖和凋亡的重要途径。IGFBP-3是影响胶质瘤发生和发展的关键细胞因子之一，且同时参与了上述通路的调节。我们研究发现GalNAc-T14能结合IGFBP-3，调节其生物功能，特别是对细胞凋亡的作用。临床样本检测表明：IGFBP-3表达升高，GalNAc-T14表达降低的患者病情较严重，并伴随ERK活化水平升高和NF-κB异常表达。本研究拟分析临床标本中GalNAc-T14、IGFBP-3及ERK和NF-κB通路中信号分子的表达和磷酸化，结合细胞系中过表达和敲低上述基因发现的ERK和NF-κB通路中信号分子的表达和活化水平的特征，阐明GalNAc-T14/IGFBP-3作用对ERK和NF-κB通路的影响及分子调控机制，为胶质瘤的治疗提供新思路和新靶点。

Glioma seriously threats to human health. The progression of glioma's pathogenetic condition is regulated by many intracellular signaling pathways, among which the ERK and NF-κB signaling pathways are two important ones that can regulate tumor cell proliferation and apoptosis. IGFBP-3 is one of the key signaling molecules that influence the generation and development of glioma. In the meantime IGFBP -3 engages in regulation of the ERK and NF-κB signaling pathways. We found that GalNAc-T14 can be combined with IGFBP-3, involved in regulating its biological function particularly its role to affect tumor cell apoptosis. Clinical sample analysis showed that patients have relatively severe disease progression when their IGFBP-3 expression was increased and GalNAc-T14 expression was reduced. Relevant, these patients are also found with increased activation of ERK signaling pathway and NF-κB expression in abnormal elevation. This study will analyze expression of GalNAc-T14 and IGFBP-3 in clinical specimens as well as expression and phosphorylation change of signaling molecules in ERK and NF-κB pathways, then combine with characteristics of expression and activation of signaling molecules in ERK and NF-κB pathways observed through overexpression and knockdown of these genes in glioma cell lines, clarify molecular regulation mechanism and the effect that interaction of GalNAc-T14/ IGFBP-3 has on ERK and NF-κB signaling pathways, eventually provide new ideas and new targets for treatment of glioma.