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GLIS 家族锌指蛋白 3 促进胶质瘤细胞的恶性行为和 NF-κB 信号通路。

GLIS family zinc finger 3 promoting cell malignant behaviors and NF-κB signaling in glioma.

机构信息

Department of Hyperbaric Oxygen, Sixth Medical Center, Chinese PLA General Hospital, No. 6 FuCheng Road, Haidian District, Beijing, China.

Department of Dermatology, The Second Hospital of Jilin University, Changchun, Jilin, China.

出版信息

Brain Res. 2021 Nov 1;1770:147623. doi: 10.1016/j.brainres.2021.147623. Epub 2021 Aug 14.

Abstract

Glioma is a common tumor in the human central nervous system. However, its molecular mechanism in the pathogenesis and regulation of glioma progression is still unclear. In this study, we found that GLIS3 was up-regulated in glioma tissues, and the increased expression is positively correlated with advanced tumor grade. Survival evaluation disclosed that patients with high expression levels of GLIS3 normally have a poor prognosis. Functional analysis revealed the oncogenic role of GLIS3 in the development of glioma. GLIS3 promotes glioma cells' invasion, migration, and proliferation. Meanwhile, deficiency of GLIS3 produces an inhibitory function upon NF-κB signaling pathway. This work demonstrated that GLIS3, acting as a target and prognostic factor for glioma, may promote the invasion, migration and proliferation of glioma cells involved in regulation of NF-κB signaling pathway.

摘要

神经胶质瘤是一种常见的人类中枢神经系统肿瘤。然而,其在发病机制和神经胶质瘤进展调控中的分子机制尚不清楚。在本研究中,我们发现 GLIS3 在神经胶质瘤组织中上调,并且表达增加与肿瘤高级别呈正相关。生存评估显示,GLIS3 高表达的患者通常预后不良。功能分析揭示了 GLIS3 在神经胶质瘤发生发展中的致癌作用。GLIS3 促进神经胶质瘤细胞的侵袭、迁移和增殖。同时,GLIS3 的缺失对 NF-κB 信号通路产生抑制作用。本工作表明,GLIS3 作为神经胶质瘤的靶点和预后因子,可能通过调控 NF-κB 信号通路促进神经胶质瘤细胞的侵袭、迁移和增殖。

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