Transmembrane emp24 domain-containing protein 3 promotes the malignant progression of glioma by regulating the ZBTB7A signaling axis.

IF 6.3 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yang Qiao, Lv Zhou, Jianyu Nie, Jinshui Li, Yangchun Hu, Peng Gao, Bingshan Wu, Hongwei Cheng, Xingliang Dai
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Abstract

Glioblastoma (GBM) is highly malignant with a poor prognosis. Exploring new therapeutic targets in GBM is an effective strategy for the prognosis of GBM patients. The Transmembrane emp24 domain-containing protein 3 (TMED3) gene has been found to play a role in the development of various cancers, but its mechanism in GBM remains unclear. This study combined the TCGA database, single-cell RNA sequencing, and in vitro and in vivo experiments to systematically investigate the role of TMED3 in GBM and its potential mechanisms. The study found that the TMED3 gene is differentially expressed in GBM samples, and high expression is associated with a higher grade of GBM and a poorer prognosis. In vitro and in vivo experiments confirmed that the upregulation of TMED3 promoted GBM proliferation, invasion, and migration. Further immunoprecipitation and functional rescue experiments revealed that Zinc finger and BTB domain-containing protein 7A (ZBTB7A) acts as a downstream target of TMED3. TMED3 promotes the malignant progression of GBM by regulating ZBTB7A. In conclusion, this study reveals that TMED3 promotes GBM development through the regulation of the ZBTB7A signaling axis, providing new insights for targeted therapy of GBM.

跨膜emp24结构域蛋白3通过调控ZBTB7A信号轴促进胶质瘤的恶性进展。
胶质母细胞瘤(GBM)是一种高度恶性且预后不良的疾病。探索新的治疗靶点是改善GBM患者预后的有效策略。跨膜emp24结构域蛋白3 (TMED3)基因已被发现在多种癌症的发展中发挥作用,但其在GBM中的机制尚不清楚。本研究结合TCGA数据库、单细胞RNA测序、体外和体内实验,系统探讨TMED3在GBM中的作用及其潜在机制。研究发现,TMED3基因在GBM样本中存在差异表达,高表达与GBM级别较高、预后较差相关。体外和体内实验证实,上调TMED3可促进GBM的增殖、侵袭和迁移。进一步的免疫沉淀和功能救援实验表明,锌指和含BTB结构域蛋白7A (ZBTB7A)是TMED3的下游靶点。TMED3通过调控ZBTB7A促进GBM恶性进展。综上所述,本研究揭示TMED3通过调控ZBTB7A信号轴促进GBM的发展,为GBM的靶向治疗提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
6.30
自引率
0.00%
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审稿时长
10 weeks
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