目的 探讨肿瘤坏死因子 α 诱导蛋白 3 相互作用蛋白 1（TNIP1）调控核因子 κB（NF⁃κB）信 号通路在 IDH 野生型胶质瘤中的作用机制。方法 使用 CGGA 和 TCGA 数据库确定 TNIP1 在 IDH 野生型 胶质瘤中的表达和预后价值。用特定的siRNA敲低了N33细胞中的TNIP1表达，并分析细胞的增殖和迁移 能力。通过免疫沉淀分析 TNIP1 与 TNF 受体相关因子 6（TRAF6）相互作用及其对 TRAF6 的泛素化影响。 分别将空载体、oe⁃TNIP1 或 si⁃TNIP1 转染的 U87 细胞注射到裸鼠的大脑中，并通过 BLI 方法监测肿瘤生长 情况。结果 TNIP1 表达与 IDH 野生型神经胶质瘤的较高恶性等级和较差的预后有关，但与 IDH 突变型 神经胶质瘤无关。TNIP1 敲低显著减弱了 N33 细胞的增殖和迁移（P < 0.05）。TNIP1 与 TRAF6 相互作用， 并且可以诱导 TRAF6 蛋白的去泛素化以激活 NF⁃κB。与空载体的异种移植物相比，oe⁃TNIP1 的异种移植 物显示出加速肿瘤进展，而 si⁃TNIP1 的异种移植物则相反。结论 TNIP1 可以诱导 TRAF6 蛋白的去泛素 化以激活NF⁃κB，进而促进IDH 野生型胶质瘤的恶性进展。

Objective To explore the mechanism of TNFα ⁃ induced protein 3 ⁃ interacting protein1 （TNIP1）in the regulation of nuclear factor kappa B （NF ⁃ κB）signaling pathway in IDH wild ⁃type glioma. Methods The CGGA and TCGA databases were used to determine the expression and prognostic value of TNIP1 in IDH wild⁃type gliomas. The expression of TNIP1 in N33 cells was knocked down with specific siRNA，and the cell proliferation and migration ability were analyzed by CCK⁃8 test，Transwell migration test，and scratch test. The interaction between TNIP1 and TNF receptor ⁃ related factor 6（TRAF6）and its influence on the ubiquitination of TRAF6 were analyzed by immunoprecipitation. U87 cells expressing an empty vector，oe⁃TNIP1 or si⁃TNIP1 were injected into the brain of nude mice，and the tumor growth was monitored by BLI method. Results TNIP1 expres⁃ sion was positively associated with a higher malignant grade and poorer prognosis of IDH⁃wild type gliomas but not IDH ⁃ mutant gliomas. TNIP1 knockdown significantly reduced the proliferation and migration of N33 cells（P < 0.05）. TNIP1 induced the deubiquitination of TRAF6，playing a pivotal role for NF⁃κB activation. Compared with empty vector xenografts，oe⁃TNIP1 xenografts accelerated tumor progression to a greater extent，whereas si⁃TNIP1 xenografts worked in an opposite way. Conclusion TNIP1 can induce the deubiquitination of TRAF6 protein to activate NF⁃κB，which in turn promotes the malignant progression of glioma.