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Purpose <p>Glioma is the most common primary brain and spinal cord tumor, with effective treatments still lacking. Stress-activated protein kinase-interacting protein 1 (<i>SIN1</i>) has been reported to be upregulated in various tumor types, contributing to tumorigenesis. However, its specific role in glioma remains unclear. This study aimed to investigate <i>SIN1’s</i> expression, clinical significance, biological functions, and underlying molecular mechanisms in glioma.</p> Methods <p><i>SIN1</i> expression and its association with clinicopathological features and prognosis were analyzed using data from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA). <i>SIN1</i> levels were quantified in glioma tissues and cell lines. The functional roles of <i>SIN1</i> were evaluated by silencing or overexpressing it in glioma cells. RNA sequencing was used to identify downstream pathways, which were further validated through in vitro experiments. Additionally, the relationship between <i>SIN1</i> and immune cell infiltration was investigated.</p> Results <p><i>SIN1</i> is aberrantly upregulated in glioma, significantly correlating with adverse clinicopathological features and poor patient prognosis. Functional studies reveal that <i>SIN1</i> upregulation enhances glioma cell proliferation and migration while suppressing apoptosis. Mechanistically, <i>SIN1</i> exerts its oncogenic effects might be through the KRAS4A/ERK pathway. Furthermore, <i>SIN1</i> expression is associated with altered immune cell infiltration within the tumor microenvironment.</p> Conclusion <p>This study identifies SIN1 as a critical oncoprotein in glioma, upregulated in tumors and associated with aggressive features and poor survival. It drives tumor progression by enhancing proliferation/migration and suppressing apoptosis might via the KRAS4A/ERK pathway, while potentially modulating immune infiltration. These findings highlight <i>SIN1</i>’s promise as a novel therapeutic target.</p>

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SIN1 facilitates glioma progression and is associated with the KRAS/ERK pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月21日

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  • Haowei Cao,
  • Zhihan Yan,
  • Mengwei Li,
  • Jing Wang,
  • Haihan Zhang,
  • Yu Cheng,
  • Jinmin Sun,
  • Jing Ren,
  • Dejun Yang

摘要

Purpose

Glioma is the most common primary brain and spinal cord tumor, with effective treatments still lacking. Stress-activated protein kinase-interacting protein 1 (SIN1) has been reported to be upregulated in various tumor types, contributing to tumorigenesis. However, its specific role in glioma remains unclear. This study aimed to investigate SIN1’s expression, clinical significance, biological functions, and underlying molecular mechanisms in glioma.

Methods

SIN1 expression and its association with clinicopathological features and prognosis were analyzed using data from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA). SIN1 levels were quantified in glioma tissues and cell lines. The functional roles of SIN1 were evaluated by silencing or overexpressing it in glioma cells. RNA sequencing was used to identify downstream pathways, which were further validated through in vitro experiments. Additionally, the relationship between SIN1 and immune cell infiltration was investigated.

Results

SIN1 is aberrantly upregulated in glioma, significantly correlating with adverse clinicopathological features and poor patient prognosis. Functional studies reveal that SIN1 upregulation enhances glioma cell proliferation and migration while suppressing apoptosis. Mechanistically, SIN1 exerts its oncogenic effects might be through the KRAS4A/ERK pathway. Furthermore, SIN1 expression is associated with altered immune cell infiltration within the tumor microenvironment.

Conclusion

This study identifies SIN1 as a critical oncoprotein in glioma, upregulated in tumors and associated with aggressive features and poor survival. It drives tumor progression by enhancing proliferation/migration and suppressing apoptosis might via the KRAS4A/ERK pathway, while potentially modulating immune infiltration. These findings highlight SIN1’s promise as a novel therapeutic target.