ArticleScientific reports2025
Identification of SUMOylation modifiers involved in lung adenocarcinoma progression and Osimertinib resistance by integrated bioinformatics analysis.
Article in Scientific reports, 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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Post-translational modifications of protein and lung cancer.Frontiers in oncology · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
This study investigates the mechanisms of Osimertinib resistance in lung adenocarcinoma (LUAD) by identifying prognostic genes associated with SUMOylation. We performed differential expression analysis to identify differentially expressed genes (DEGs) in LUAD samples, Osimertinib-tolerant cell samples and SUMOylation-related genes (SRGs). Utilizing Cox regression and LASSO regression, we developed a prognostic model that highlighted five key prognostic genes-BIRC5, AURKA, BLM, NR3C2, and NDC1. These genes were significantly associated with LUAD progression, revealing their predominant expression in epithelial cells, which play a vital role in tumor development. Furthermore, we explored the biological functions and signaling pathways linked to these prognostic genes, discovering that their expression levels and corresponding risk scores could serve as indicators of CD4 T cell and memory B cell activation. The enriched signaling pathways in LUAD were regulated by ubiquitin-related small modifiers, highlighting the complex interplay between SUMOylation and tumor biology. Our findings suggest the important role of SUMOylation-regulated genes in LUAD progression and Osimertinib resistance, suggesting their potential as valuable biomarkers for prognosis and therapeutic targets to enhance treatment strategies for patients with EGFR-mutant lung adenocarcinoma.
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