Geng Zhi, Mu Chunyan, Qiu Yuxiang, Tang Yuchen, Su Mingyu, Tang Chuanxi, Zhang Lei
Department of Pediatric Surgery, Tengzhou Central People's Hospital, Tengzhou, Shandong, China.
Department of Neurobiology, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Front Mol Neurosci. 2024 Jul 31;17:1438135. doi: 10.3389/fnmol.2024.1438135. eCollection 2024.
Coatomer 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.
The 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 experiments to evaluate the functional role and mechanism of COPZ2 in glioma cell lines.
We 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.
Our 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.
衣被蛋白复合物ζ2（COPZ2）是七聚体衣被蛋白复合物I的成员，据报道其参与多种肿瘤。然而，COPZ2在胶质瘤中的潜在作用仍有待探索。
从癌症基因组图谱（TCGA）获取COPZ2表达及相关临床数据。利用TIMER2.0和Ualcan数据库评估COPZ2在各种肿瘤中的表达。进行单变量、多变量Cox回归、Kaplan-Meier方法、列线图分析和ROC曲线分析，以评估COPZ2和其他预后因素与胶质瘤的关系。使用LinkedOmics数据库预测COPZ2在胶质瘤中的潜在生物学机制。我们还进行了实验，以评估COPZ2在胶质瘤细胞系中的功能作用和机制。
我们发现COPZ2在胶质瘤中高表达，且与年龄和世界卫生组织分级相关。Kaplan-Meier生存曲线、Cox分析、列线图分析和ROC曲线显示，COPZ2是胶质瘤预后不良的不利因素。COPZ2及其共表达基因的功能与中性粒细胞介导的免疫、粒细胞活化和对干扰素-γ的反应显著相关。此外，敲低COPZ2可显著抑制胶质母细胞瘤细胞的增殖、迁移和侵袭。机制上，COPZ2通过参与PI3K-AKT信号通路的调节来抑制肿瘤发展。
我们的结果表明，COPZ2的升高与胶质瘤的预后和进展相关，它可能是胶质瘤潜在的诊断和预后生物标志物。
