ArticleOncology letters2025
Prognostic role and mutational characteristics of N6-methyladenosine-related genes in lung adenocarcinoma.
Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Multi-omics and network pharmacology identify IGFBP1 as an m6A-Epigenetic target of pueraria in NSCLC therapy.PLoS computational biology · 2026Article
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5 authors.
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Abstract
Lung adenocarcinoma (LUAD) is an invasive disease that originates from small airway epithelial cells or alveolar type II cells. Abnormal N6-methyladenosine (m6A) RNA methylation serves a key role in the pathogenesis of human diseases, including cancer. RNA sequencing and somatic mutation data in the Genomic Data Commons (GDC) and The Cancer Genome Atlas (TCGA)-LUAD were downloaded from University of California, Santa Cruz (UCSC) Xena database for a comprehensive analysis. m6A-related genes were selected from the content of RNA m6A modification in cancer. m6A genes were further screened by comparing how m6A genes affected survival in normal and tumor groups and analyzing the relationship between m6A genes and LUAD. GDC LUAD data were downloaded from the UCSC Xena public database to analyze the differential expression levels of genes involved with m6A methylation regulators. Next, the mutations of m6A genes were analyzed and a univariate Cox regression analysis and the Kaplan-Meier method were used to determine the relationship between their expression levels and overall survival time shown in TCGA database. Lastly, heterogeneous nuclear ribonucleoprotein C (HNRNPC), insulin-like growth factor 2 mRNA binding protein (IGF2BP)1 and IGF2BP3 were selected for subsequent analysis. Enrichment analysis revealed that HNRNPC was mainly enriched in the 'ribonucleoprotein complex biogenesis' pathway, IGF2BP1 in the 'mitotic cell cycle checkpoint' pathway and IGF2BP3 in the 'nuclear division' pathway. The present study identified novel immune-related prognostic markers for LUAD. Furthermore, the potential mechanisms of the prognostic markers in the regulation of LUAD etiology were investigated. The present study findings may provide novel insights into the treatment of patients with LUAD in the future.
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