Comprehensive analysis of the prognostic role and mutational characteristics of m6A-related genes in lung adenocacinoma

Abstract

Abstract Background Lung adenocarcinoma (LUAD) is an invasive disease, which originates from small airway epithelial cells or alveolar type II cells. N6-methyladenosine (M6A) RNA methylation is involved in diverse biological processes. Studies have shown that m6A RNA methylation abnormalities play an important role in the pathogenesis of many human diseases, including cancer. The present study explores the prognostic role and mutational characteristics of m6A-related genes in LUAD. Methods RNA-seq and somatic mutation data of Genomic Data Commons and The Cancer Genome Atlas (GDC TCGA)-LUAD were downloaded from UCSC Xena for comprehensive analysis. M6A-related genes were selected from the content of RNA m6A modification in cancer. M6A genes were further screened by comparing the significance and survival of m6A genes between the normal group and the tumor group and analyzing the relationship between m6A genes and LUAD patients. Results GDC LUAD data were downloaded from UCSC Xena public database, and the gene expression data of 19 m6A methylation regulators in LUAD were extracted for differential expression levels. Then, the mutation of m6A genes was analyzed based on the single nucleotide polymorphism data of UCSC Xena. To further confirm the prognostic genes, univariate Cox regression and the Kaplan Meier method were used to determine the relationship between their expression level and the overall survival time in the TCGA database. Finally, HNRNPC, IGF2BP1, and IGF2BP3 genes were established for subsequent analysis. Correlation analyses showed that the three genes were correlated with clinical features and immune cell infiltration. Enrichment analysis revealed that HNRNPC was mainly enriched in ribonucleoprotein complex biogenesis, IGF2BP1 in the mitotic cell cycle checkpoint, and IGF2BP3 in the nuclear division pathway. Conclusions Our study identified novel immune-related prognostic markers of LUAD. Moreover, the potential mechanisms of prognostic markers in regulating the etiology of LUAD were investigated. These findings enrich our understanding of the relationships between immune and LUAD and may provide new insights into the treatment of LUAD patients.