Tripartite motif-containing 25 facilitates immunosuppression and inhibits apoptosis of glioma via activating NF-κB

被引:6
作者
Ge, Mao-xu [1 ]
Shi, Yi-kang [2 ]
Liu, Dong [3 ,4 ,5 ]
机构
[1] Shandong Univ, Dept Pharm, Qilu Hosp, Jinan 250012, Peoples R China
[2] Shandong Univ, Natl Glycoengn Res Ctr, Qingdao 266237, Peoples R China
[3] Shandong First Med Univ, Inst Pharmacol, Tai An 271016, Shandong, Peoples R China
[4] Shandong Acad Med Sci, Tai An 271016, Shandong, Peoples R China
[5] Shandong First Med Univ, Coll Pharm, Tai An 271016, Shandong, Peoples R China
关键词
TRIM25; glioma; immune suppression; apoptosis; NF-kappa B; TRIM25; PROMOTES; CELL-SURVIVAL; IMMUNOTHERAPY; MACROPHAGES; EXPRESSION; MICROENVIRONMENT; BIOLOGY; GROWTH; ALPHA;
D O I
10.1177/15353702221099460
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
As a crucial tumor type of the central nervous system, gliomas are characterized by a dismal prognosis. Tripartite motif-containing 25 (TRIM25), an essential E3 ubiquitin ligase, participates in various biological processes. This study sought to demonstrate its functional role in gliomas. Data obtained from publicly available databases - including The Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA), and the Repository for Molecular Brain Neoplasia Data (REMBRANDT) - were employed. TRIM25 expression pattern and its association with different clinical characteristics were analyzed. Kaplan-Meier analysis was utilized to compare different TRIM25 expressions with glioma patients' survival. Subsequently, we performed bioinformatic analyses to investigate the biological functions of TRIM25, which were further validated by in vitro experiments, CIBERSORT algorithm, and ESTIMATE evaluation. TRIM25 expression was upregulated in glioma patients and can predict an unfavorable prognosis. Bioinformatic results indicated the involvement of TRIM25 in apoptosis and immune regulation. TRIM25 was associated with programmed death-ligand 1 (PD-L1) related and macrophage-induced immune suppression in gliomas. Meanwhile, silencing TRIM25 promoted apoptosis in glioma cells, which is attributed to its regulation of NF-kappa B. Therefore, TRIM25 contributed to the glioma malignant progression and suppressive immune microenvironments via NF-kappa B activation, which may play a therapeutic role in gliomas.
引用
收藏
页码:1529 / 1541
页数:13
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