The study looked at genes involved in a chemical process called palmitoylation and how they affect lung cancer outcomes and immune cell presence in tumors. It identified five genes that can predict patient risk, showed that high‑risk patients have fewer immune cells in their tumors, and split lung cancer into two sub‑types with different molecular features. The work is purely computational and does not test any actual peptide or supplement.

Lung adenocarcinoma (LUAD), which is the most frequently diagnosed form of lung cancer, constitutes a major global health challenge due to its significant mortality rate. Palmitoylation, as a key post-translational modification of proteins, plays an important role in tumor progression. However, its influence on sculpting the tumor immune microenvironment (TME) and its subsequent impact on patient prognosis remains incompletely understood. This study was based on the TCGA-LUAD and GSE72094 cohort data sets to explore the potential role of palmitoylation-related genes (PRGs) in LUAD. Through the integration of differential analysis, weighted gene coexpression network analysis (WGCNA), univariate Cox analysis and least absolute shrinkage and selection operator (LASSO) regression analysis, prognostic genes for LUAD were screened. Furthermore, the infiltration patterns of immune cells across different groups were assessed by applying the ssGSEA and CIBERSORT algorithms. To elucidate the potential biological processes mediated by PRGs in LUAD pathogenesis, GSEA, GO and KEGG enrichment analyses, were used. In addition, the consensus clustering method was utilized for identify molecular subtypes of LUAD. This study identified 5 PRGs as prognostic genes for LUAD and constructed a robust prognostic model. Immune infiltration analysis indicated that the level of immune cell infiltration in patients of the high-risk group was significantly lower. Further enrichment analysis showed that the upregulated differentially expressed genes (DEGs) in the high and low risk groups were related to the cytoskeleton, while the downregulated DEGs were related to lipid metabolism. In addition, this study successfully classified LUAD into 2 molecular subtypes with significant differences. Our research delves into the intricate TME and molecular mechanisms of LUAD, providing new insights into the pathologic mechanism and treatment strategies of LUAD.