Abstract
Lung adenocarcinoma (LUAD) is one of the leading global health challenges wherein novel therapeutic targets are much needed. In this systems bioinformatics study, we report that disruption of the long noncoding RNA (lncRNA) SFTA1P-centered network, respiratory gaseous exchange and surfactant-associated Biological Network (rgsBNet), is consistent with impairing surfactant homeostasis and respiratory function, and thus warrants attention for future drug discovery and development. We analyzed data from The Cancer Genome Atlas LUAD cohort to identify differentially expressed mRNAs, lncRNAs, and microRNAs (miRNAs), followed by correlational analysis to examine the coexpression network of lncRNA SFTA1P and its potential role in LUAD pathogenesis. We observed the downregulation of lncRNA SFTA1P and its coexpressed network in LUAD. Intriguingly, this network appears to be associated with disrupting surfactant homeostasis and perturbing respiratory function, suggesting a potential role in LUAD progression. Additionally, we identified key transcription factors that correlate with the expression of genes crucial for respiratory gaseous exchange and surfactant homeostasis. The attendant regulatory mechanisms suggested that SFTA1P may act as a “sponge” for certain miRNAs, sequestering them away from their mRNA targets. In conclusion, this work uncovers novel insights into the molecular mechanisms governing surfactant homeostasis in LUAD and offers a possible avenue for therapeutic interventions aimed at ameliorating lung function and improving disease management. The downregulation of lncRNA SFTA1P and its coexpressed network highlights their potential as regulators of lung function and opens doors for further investigation into their role in LUAD progression and as potential therapeutic targets.
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