N6‐methyladenine‐related genes affect biological behavior and the prognosis of glioma

BACKGROUND: Although aberrant expression of N6‐methyladenine (m(6)A) methylation‐related genes contribute to tumorigenesis in many solid tumors, the prognostic value of the m(6)A‐related genes and their correlation with clinicopathological features in gliomas need advanced study. METHODS: The clinical and sequencing data of 288 patients with glioma were extracted from Chinese Glioma Genome Atlas database. By univariate and multivariable Cox regression analysis, the m(6)A‐related prognostic genes were identified, and their correlation with clinicopathological features was further analysis. A nomogram was constructed by R software and the performance of it was assessed by calibration and time‐dependent receiver operating characteristic curve. RESULTS: Nine m(6)A‐related genes were identified as independent prognostic factors, which were mostly enriched in RNA splicing, regulation of immune response and vesicle‐mediated transport. By expression value and regression coefficient of these genes, we constructed risk score of each patient, which was highly associated with clinicopathological features. Kaplan–Meier curve showed that the prognosis of patients with high‐risk scores was significantly worse than that with low‐risk scores (HR = 4.30, 95% CI = 3.16–5.85, p < 0.0001). A nomogram was constructed based on the nine m(6)A‐related genes signature and clinicopathological features with well‐fitted calibration curves (c‐index = 0.82), showing high specificity and sensitivity (area under the curve for 1‐, 3‐, and 5‐years survival probability = 0.874, 0.918, and 0.934). CONCLUSIONS: A nine m(6)A‐related genes signature was identified in gliomas. The m(6)A‐related risk score is a novel prognostic factor for patients with glioma, and is associated with clinicopathological features. Moreover, the nomogram based on the nine m(6)A‐related genes signature and clinicopathological features had good efficacy in predicting the survival probability.