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<p>Calcium/calmodulin-dependent protein kinase IIα (CAMK2A) is a ubiquitous mediator of Ca²⁺ signal transduction, implicated in the regulation of tumor cell proliferation and differentiation. However, its role and underlying mechanism in glioma remain unclear. In this study, CAMK2A gene expression was analyzed through various glioma-related databases, and confirmed by RT qPCR and Western blotting. Compared with normal brain tissue, CAMK2A expression in glioma tissue was significantly downregulated, with expression levels progressively decreasing as tumor grade increased. Kaplan-Meier survival analysis revealed a significant correlation between low CAMK2A expression and shorter overall survival in glioma patients. The correlation analysis of CAMK2A expression with clinicopathological characteristics revealed that low expression of CAMK2A was significantly associated with tumor recurrence, high pathological grade, TMZ treated, IDH wild-type status, and 1p19q non-codeletion. Enrichment analysis indicated that in the low CAMK2A expression group, biological functions related to calcium signaling pathway, neuroactive ligand-receptor interaction and long-term potentiation were activated. The correlation analysis of CAMK2A expression with the immune microenvironment revealed that the expression level of CAMK2A influenced the immune activity of the TME. CAMK2A expression was negatively correlated with the immune score. Additionally, CAMK2A expression was correlated with multiple immune checkpoint molecules. A significant negative correlation was also observed between CAMK2A expression and TMB. Furthermore, there were associations with Macrophages M0, Plasma cells, T cells regulatory, Dendritic cells activated and T cells gamma delta. All immunobiological functions in the CAMK2A low-expression group were significantly upregulated. Functional CCK-8 assays confirmed that overexpression of CAMK2A inhibited the proliferation of glioma cells, whereas CAMK2A gene knockout produced the opposite effect. Additionally, we discovered that CAMK2A regulates glioma cell proliferation by inhibiting the Ras/Raf/MEK/ERK pathway. In summary, our findings support the notion that CAMK2A is low expressed in gliomas, and this low expression is closely associated with poor prognosis and the immune microenvironment of gliomas. CAMK2A regulates glioma cell proliferation through the Ras/Raf/MEK/ERK signaling pathway. CAMK2A is a potentially important target for glioma therapy.</p>

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A novel glioma prognosis marker CAMK2A is related to immune microenvironment and may be involved in Ras/Raf/MEK/ERK signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月25日

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  • Zhimin Sun,
  • Jiamin Zhang,
  • Qianxu Jin,
  • Aobo Zhang,
  • Zhigang Yao,
  • Zongmao Zhao,
  • Zhizhao Ma,
  • Jie Hu

摘要

Calcium/calmodulin-dependent protein kinase IIα (CAMK2A) is a ubiquitous mediator of Ca²⁺ signal transduction, implicated in the regulation of tumor cell proliferation and differentiation. However, its role and underlying mechanism in glioma remain unclear. In this study, CAMK2A gene expression was analyzed through various glioma-related databases, and confirmed by RT qPCR and Western blotting. Compared with normal brain tissue, CAMK2A expression in glioma tissue was significantly downregulated, with expression levels progressively decreasing as tumor grade increased. Kaplan-Meier survival analysis revealed a significant correlation between low CAMK2A expression and shorter overall survival in glioma patients. The correlation analysis of CAMK2A expression with clinicopathological characteristics revealed that low expression of CAMK2A was significantly associated with tumor recurrence, high pathological grade, TMZ treated, IDH wild-type status, and 1p19q non-codeletion. Enrichment analysis indicated that in the low CAMK2A expression group, biological functions related to calcium signaling pathway, neuroactive ligand-receptor interaction and long-term potentiation were activated. The correlation analysis of CAMK2A expression with the immune microenvironment revealed that the expression level of CAMK2A influenced the immune activity of the TME. CAMK2A expression was negatively correlated with the immune score. Additionally, CAMK2A expression was correlated with multiple immune checkpoint molecules. A significant negative correlation was also observed between CAMK2A expression and TMB. Furthermore, there were associations with Macrophages M0, Plasma cells, T cells regulatory, Dendritic cells activated and T cells gamma delta. All immunobiological functions in the CAMK2A low-expression group were significantly upregulated. Functional CCK-8 assays confirmed that overexpression of CAMK2A inhibited the proliferation of glioma cells, whereas CAMK2A gene knockout produced the opposite effect. Additionally, we discovered that CAMK2A regulates glioma cell proliferation by inhibiting the Ras/Raf/MEK/ERK pathway. In summary, our findings support the notion that CAMK2A is low expressed in gliomas, and this low expression is closely associated with poor prognosis and the immune microenvironment of gliomas. CAMK2A regulates glioma cell proliferation through the Ras/Raf/MEK/ERK signaling pathway. CAMK2A is a potentially important target for glioma therapy.