ORIGINAL RESEARCH article
Front. Genet.
Sec. Cancer Genetics and Oncogenomics
Volume 16 - 2025 | doi: 10.3389/fgene.2025.1655262
This article is part of the Research TopicAdvancing Non-small Lung Cancer Management Through Biomarker IntegrationView all 6 articles
Identification and validation of selenium metabolism-related genes in lung adenocarcinoma prognosis using bioinformatics analysis
Provisionally accepted- 1The First People's Hospital of Yunnan Province, Kunming, China
- 2Affiliated Calmette Hospital of Kunming Medical University, Kunming, China
- 3The First People’s Hospital of Yunnan Province, Kunming, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: The disruption of selenium metabolism has been associated with tumor progression. However, the prognostic significance and underlying molecular mechanisms of selenium metabolism in lung adenocarcinoma (LUAD) remain inadequately understood. This study primarily aimed to identify and validate prognostic genes related to selenium metabolism in LUAD patients. Methods: Transcriptomic datasets from patients diagnosed with LUAD were meticulously analyzed to identify differentially expressed genes associated with selenium metabolism. The genes selected for the prognostic risk model were determined through various analyses, including differential gene expression assessment, univariate and multivariate Cox proportional hazards regression analyses, as well as other relevant analytical methods. A systematic approach was employed for functional enrichment analysis, characterization of the immune microenvironment, somatic mutation analysis, and evaluation of drug sensitivity to elucidate the mechanisms linked to prognostic genes and risk categories. Finally, a reverse transcription quantitative PCR(RT-qPCR) assay was conducted to validate the expression levels of the identified prognostic genes. Results: F2, GPX3, KMO, and KYNU were identified as prognostic genes for establishing a risk model. The functions of these LUAD prognostic genes were influenced by DNA replication pathways, cell cycle regulation, and quiescent CD4 memory T cells. In the high-risk group(HRG), KEAP1, TTN, and USH2A exhibited the highest mutation rate at 48%, while TTN had an even higher mutation rate of 52% in the low-risk group (LRG). Within the HRG cohort, both cisplatin and gemcitabine demonstrated significant sensitivity. Ultimately, RT-qPCR findings corroborated results obtained from bioinformatics analyses; specifically compared to normal samples: GPX3, KMO, KYNU showed significant downregulation in LUAD tissues while F2 was found to be upregulated in LUAD. Conclusion: This study identified four prognostic genes in LUAD and examined their associated mechanisms of action, which may contribute to the development of novel treatment strategies. The integration of immune characterization with drug sensitivity analysis offers valuable insights for stratified therapy.
Keywords: Lung Adenocarcinoma, selenium metabolism, Prognostic model, Tumor Microenvironment, Immunotherapy response, drug sensitivity
Received: 12 Jul 2025; Accepted: 06 Oct 2025.
Copyright: © 2025 Chen, Li, Wang, Shen, Chen, Peng and Xu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Zheyuan Xu, 640039365@qq.com
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.