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Abstract
BackgroundLung adenocarcinoma (LUAD) is a deadly respiratory system malignancy with poor prognosis. Autophagy is essential for the beginning, development, and therapy resistance of cancer. However, the expression of genes participating in autophagy in LUAD and their associations with prognosis remain unclear.MethodsPredictive genes participating in autophagy in LUAD samples from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets were investigated. TCGA and GEO cohorts were divided into two risk groups, while the low-risk group having a longer overall survival (OS) time. This article aims to point out the interaction between genes participating in autophagy and immune function, immune checkpoints, and m6a in LUAD. The prediction model was designed for exploring least absolute shrinkage and selection operator (LASSO) regression. It has been revealed that gene expression and autophagy are inextricably connected.ResultsGenes participating in autophagy were shown to be somewhat overexpressed in the high-risk group even though no different clinical symptoms were present, indicating that they might be used in a model to predict LUAD prognosis. The majority of genes participating in autophagy prognostic signatures controlled immunological and tumor-related pathways, according to gene set enrichment analysis (GSEA). KRT6A, KYNU, IGFBP1, DKK1, PKP2, PLEK2, GAPDH, FLNC, and NTSR1 might be related to the oncology process for LUAD patients. CERS4, CMAHP, and PLEKHB1 have been identified as being associated with low risk in patients with LUAD. Furthermore, the immune function and m6a gene expression differed significantly between the two groups.ConclusionsGenes participating in autophagy are connected to the development and progression of LUAD. LUAD patients’ prognoses are often foreseen utilizing matched prognostic models. Genes participating in autophagy in LUAD may be therapeutic targets that ought to be investigated more.
Highlights
Lung adenocarcinoma (LUAD) may be a leading reason for cancer-related death globally
Understanding, the impact of genes participating in autophagy on LUAD development may invent a biomarker that might be utilized as Abbreviations: LUAD, lung adenocarcinoma; GO, Gene Ontology; AUC, area under the curve; MF, molecular functions; ICIs, immune checkpoint inhibitors; receiver operating characteristics (ROC), receiver operating characteristic; GSEA, gene set enrichment analysis; KEGG, Kyoto Encyclopedia of Genes and Genomes; TCGA, The Cancer Genome Atlas; Immune checkpoint-related gene (ICRG), immune checkpoint-related gene; Biological processes (BP), biological processes; CC, cellular components; OS, overall survival; GEO, Gene Expression Omnibus; DEGs, differentially expressed genes
Twenty-five participating in autophagy DEGs to 12 risk genes participating in autophagy were found
Summary
Lung adenocarcinoma (LUAD) may be a leading reason for cancer-related death globally. Yoshinori Ohsumi [7] highlighted the essential principle: autophagy is essential for eliminating “garbage” from cells, preventing aberrant death and protecting traditional cell functioning. It is a cell self-defense and selfrenewal method that depends on lysosomes to destroy their organelles or proteins [8, 9]. Rare sequence-based studies on aberrant gene expression and its relationship to overall survival (OS) in LUAD patients with autophagy were conducted. The expression of genes participating in autophagy in LUAD and their associations with prognosis remain unclear
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