Abstract
BackgroundGlioma is the most common primary intracranial tumour and has a very poor prognosis. Pyroptosis, also known as inflammatory necrosis, is a type of programmed cell death that was discovered in recent years. The expression and role of pyroptosis-related genes in gliomas are still unclear.MethodsIn this study, we analysed the RNA-seq and clinical information of glioma patients from The Cancer Genome Atlas (TCGA) database and Chinese Glioma Genome Atlas (CGGA) database. To investigate the prognosis and immune microenvironment of pyroptosis-related genes in gliomas, we constructed a risk model based on the TCGA cohort. The patients in the CGGA cohort were used as the validation cohort.ResultsIn this study, we identified 34 pyroptosis-related differentially expressed genes (DEGs) in glioma. By clustering these DEGs, all glioma cases can be divided into two clusters. Survival analysis showed that the overall survival time of Cluster 1 was significantly higher than that of Cluster 2. Using the TCGA cohort as the training set, a 10-gene risk model was constructed through univariate Cox regression analysis and LASSO Cox regression analysis. According to the risk score, gliomas were divided into high-risk and low-risk groups. Survival analysis showed that the low-risk group had a longer survival time than the high-risk group. The above results were verified in the CGGA validation cohort. To verify that the risk model was independent of other clinical features, the distribution and the Kaplan-Meier survival curves associated with risk scores were performed. Combined with the characteristics of the clinical cases, the risk score was found to be an independent factor predicting the overall survival of patients with glioma. The analysis of single sample Gene Set Enrichment Analysis (ssGSEA) showed that compared with the low-risk group, the high-risk group had immune cell and immune pathway activities that were significantly upregulated.ConclusionWe established 10 pyroptosis-related gene markers that can be used as independent clinical predictors and provide a potential mechanism for the treatment of glioma.
Highlights
Glioma accounts for most primary malignant brain tumours with high levels of mortality and aggressiveness in the central nervous system [1, 2]
Great progress has been made in the molecular pathology of nervous system malignant tumours, and a series of molecular markers, such as MGMT promoter methylation, IDH mutations, chromosome 1p/19q co-deletion and TERT promoter mutations, have been found that are helpful for the clinical diagnosis and prediction of the formation, invasion, progression and prognosis of glioma [7, 8]
Identification of differentially expressed pyroptosis genes in gliomas and normal brain tissues The 51 pyroptosis-related genes expression were compared in 1152 normal brain tissues (GTEx) and 667 glioma tissues (TCGA), and we identified 45 differentially expressed genes (DEGs) (Fig. 1B)
Summary
Glioma accounts for most primary malignant brain tumours with high levels of mortality and aggressiveness in the central nervous system [1, 2]. Great progress has been made in the molecular pathology of nervous system malignant tumours, and a series of molecular markers, such as MGMT promoter methylation, IDH mutations, chromosome 1p/19q co-deletion and TERT promoter mutations, have been found that are helpful for the clinical diagnosis and prediction of the formation, invasion, progression and prognosis of glioma [7, 8] Among these molecular markers, IDH1, 1p19q, and MGMT methylation have been closely associated with the prognosis and chemotherapy sensitivity of glioma patients, these markers have limited sensitivity and accuracy [9]. The expression and role of pyroptosis-related genes in gliomas are still unclear
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