Abstract
BackgroundGrowth arrest–specific 2 like 3 (GAS2L3) is a cytoskeleton-associated protein that interacts with actin filaments and tubulin. Abnormal GAS2L3 expression has been reported to be associated with carcinogenesis. However, the biological role of GAS2L3 in glioma remains to be determined.MethodsThe transcriptome level of GAS2L3 and its relationship with clinicopathological characteristics were analyzed among multiple public databases and clinical specimens. Bioinformatics analyses were conducted to explore biological functions and prognostic value of GAS2L3 in glioma.ResultsGAS2L3 was substantially expressed in glioma, and high GAS2L3 expression correlated with shorter overall survival time and poor clinical variables. Gene set enrichment analysis (GSEA), single-sample gene-set enrichment analysis, and CIBERSORT algorithm analyses showed that GAS2L3 expression was closely linked to immune-related pathways, inflammatory activities, and immune cell infiltration. Moreover, GAS2L3 was synergistic with T cell–inflamed gene signature, immune checkpoints, T-cell receptor diversities, and neoantigen numbers.ConclusionThis study suggests that GAS2L3 is a prognostic biomarker for glioma, providing a reference for further study of the potential role of GAS2L3 in the immunomodulation of glioma.
Highlights
Worldwide, gliomas account for approximately 40–50% of all neoplasms of the central nervous system (CNS) (Ostrom et al, 2018)
Growth arrest–specific 2 like 3 (GAS2L3) was significantly upregulated in brain and CNS, breast cancer, gastric cancer, kidney cancer, and pancreatic cancer, but downregulated in leukemia (Figure 1A)
These results suggest that the high expression of GAS2L3 is common in various types of cancer
Summary
Gliomas account for approximately 40–50% of all neoplasms of the central nervous system (CNS) (Ostrom et al, 2018). It has been reported that GAS2L3 was dysregulated in various tumor cells. Shi et al (2020) reported that GAS2L3 was significantly related to the deterioration of overall survival (OS) and disease-free survival in hepatocellular carcinoma. Seidl et al (2010) reported that GAS2L3 was downregulated after incubation with highly cytotoxic α-emitter immunoconjugates in gastric cancer cells. The role of GAS2L3 in glioma has not been reported. Growth arrest–specific 2 like 3 (GAS2L3) is a cytoskeleton-associated protein that interacts with actin filaments and tubulin. Abnormal GAS2L3 expression has been reported to be associated with carcinogenesis. The biological role of GAS2L3 in glioma remains to be determined
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