Identification and analysis of amino acid metabolism-related subtypes in lung adenocarcinoma.

Abstract

We aimed to explore the role of amino acid metabolism (AAM) and identify biomarkers for prognosis management and treatment of lung adenocarcinoma. Differentially expressed genes (DEGs) associated with AAM in lung adenocarcinoma were selected from public databases. Samples were clustered into varying subtypes using ConsensusClusterPlus based on gene levels. Survival analysis was conducted using a survival package, and immune analysis was performed using ssGSEA and ESTIMATE. Enrichment analysis was performed using gene set enrichment analysis, and a protein-protein interaction network of DEGs between subgroups was established through STRING. Hub genes were screened and verified using survival analysis, and drug sensitivity prediction was performed. One hundred sixty-three DEGs associated with AAM in lung adenocarcinoma were obtained, and two AAM-associated subtypes were identified. Cluster 1 showed higher survival rates and immune levels compared with cluster 2. The two subtypes were mainly enriched in immune-related signaling pathways, such as B cell receptor, Jak-Stat, and natural killer cell-mediated cytotoxicity. In addition, the mutation landscape between the two groups was significantly different. F2, AHSG, and APOA1 were key hub genes that significantly affected the prognosis differences between the two subtypes. Cluster 2 showed higher sensitivity to drugs, such as mithramycin, depsipeptide, and actinomycin than cluster 1. This study identified two AAM-associated gene subtypes and their biomarkers and predicted the immune status and drug treatment sensitivity of varying subtypes. The results are instructive in the clinical treatment of lung adenocarcinoma.NEW & NOTEWORTHY Two amino acid metabolism-related subtypes were identified based on differentially expressed genes associated with amino acid metabolism. Cluster 1 showed higher survival rates and immune levels compared with cluster 2. Cluster 2 showed higher sensitivity to drugs, such as mithramycin, depsipeptide, and actinomycin compared with cluster 1.