COPZ2 的高表达与胶质瘤的不良预后和癌症进展有关

IF 3.5 3区 医学 Q2 NEUROSCIENCES Frontiers in Molecular Neuroscience Pub Date : 2024-07-31 DOI:10.3389/fnmol.2024.1438135
Zhi Geng, Chunyan Mu, Yuxiang Qiu, Yuchen Tang, Mingyu Su, Chuanxi Tang, Lei Zhang
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引用次数: 0

摘要

背景衣壳蛋白复合物zeta 2(COPZ2)是七聚体衣壳蛋白复合物I的成员之一,有报道称其参与多种肿瘤的研究。方法COPZ2的表达及相关临床数据来自癌症基因组图谱(TCGA)。利用TIMER2.0和Ualcan数据库评估COPZ2在不同肿瘤中的表达。通过单变量、多变量Cox回归、Kaplan-Meier方法、提名图分析和ROC曲线分析来评估COPZ2和其他预后因素与胶质瘤的关系。我们利用 LinkedOmics 数据库预测了 COPZ2 在胶质瘤中的潜在生物学机制。我们还进行了体外实验,以评估 COPZ2 在胶质瘤细胞系中的功能作用和机制。Kaplan-Meier生存曲线、Cox分析、提名图分析和ROC曲线显示,COPZ2是胶质瘤不良预后的不利因素。COPZ2和共表达基因的功能与中性粒细胞介导的免疫、粒细胞活化和对γ干扰素的反应显著相关。此外,敲除 COPZ2 能显著抑制胶质母细胞瘤细胞的增殖、迁移和侵袭。结论我们的研究结果表明,COPZ2的升高与胶质瘤的预后和进展有关,它可能是胶质瘤潜在的诊断和预后生物标志物。
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High expression of COPZ2 is associated with poor prognosis and cancer progression in glioma
BackgroundCoatomer protein complex zeta 2 (COPZ2) is a member of heptameric coatomer protein complex I and has been reported to be involved in various tumors. However, COPZ2’s potential involvement in glioma remains to be explored.MethodsThe COPZ2 expression and related clinical data were obtained from The Cancer Genome Atlas (TCGA). TIMER2.0 and the Ualcan database were utilized to assess the COPZ2 expression in various tumors. Univariable, multivariate Cox regression, Kaplan–Meier methods, nomogram analysis, and ROC curve analysis were carried out to assess the relationship of COPZ2 and other prognostic factors with glioma. The LinkedOmics database was used to predict the potential biological mechanism of COPZ2 in glioma. We also conducted in vitro experiments to evaluate the functional role and mechanism of COPZ2 in glioma cell lines.ResultsWe found that COPZ2 was highly expressed in glioma and it was associated with age and WHO grades. Kaplan–Meier survival curves, Cox analysis, nomogram analysis, and ROC curve showed that COPZ2 was a disadvantageous factor in poor glioma prognosis. The functions of COPZ2 and co-expression genes were significantly associated with neutrophil-mediated immunity, granulocyte activation, and response to interferon-gamma. In addition, COPZ2 knockdown significantly inhibited the proliferation, migration, and invasion of glioblastoma cells. Mechanistically, COPZ2 suppressed tumor development by participating in the regulation of the PI3K-AKT signaling pathway.ConclusionOur results demonstrated that the elevation of COPZ2 was associated with the prognosis and progression of glioma, and it might be a potential diagnostic and prognostic biomarker for glioma.
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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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