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ORIGINAL RESEARCH article

Front. Mol. Neurosci.
Sec. Molecular Signalling and Pathways
Volume 17 - 2024 | doi: 10.3389/fnmol.2024.1438135
This article is part of the Research Topic Molecular pathology, biomarkers and therapeutics of brain tumor and neurodegenerative disease View all 3 articles

High expression of COPZ2 is associated with poor prognosis and cancer progression in glioma

Provisionally accepted
Zhi Geng Zhi Geng 1Chunyan Mu Chunyan Mu 2Yuxiang Qiu Yuxiang Qiu 2Yuchen Tang Yuchen Tang 2Chuanxi Tang Chuanxi Tang 2Lei Zhang Lei Zhang 3*
  • 1 Tengzhou City Center People's Hospital, Zaozhuang, Shandong Province, China
  • 2 Xuzhou Medical University, Xuzhou, Jiangsu Province, China
  • 3 The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China

The final, formatted version of the article will be published soon.

    Background: 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 in vitro experiments to evaluate the functional role and mechanism of COPZ2 in glioma cell lines.Results: 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.

    Keywords: Glioma, COPZ2, prognosis, Migration, proliferation

    Received: 25 May 2024; Accepted: 08 Jul 2024.

    Copyright: © 2024 Geng, Mu, Qiu, Tang, Tang and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Lei Zhang, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.