ArticlePeerJ2026
Nicotine-induced immune escape mechanisms in lung adenocarcinoma: ceRNA network toxicology, and molecular dynamics simulations.
Article in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
8 authors.
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Abstract
Lung adenocarcinoma (LUAD), the most common subtype of lung cancer and a leading cause of cancer-related deaths, is strongly associated with cigarette smoking and nicotine exposure. However, the molecular mechanisms underlying nicotine-induced LUAD remain unclear. This study employed an integrative approach combining network toxicology, competing endogenous RNA (ceRNA) analysis, molecular docking, and dynamics simulations to investigate nicotine's role in LUAD. Network toxicology identified 81 potential nicotine targets, with 12 core targets showing significant differential expression in LUAD. Functional enrichment suggested involvement of immune escape, inflammation, and cell death. A ceRNA network highlighted microRNA-101 and microRNA-155-5p as key regulators. Molecular docking and dynamics simulations demonstrated stable binding between nicotine and core targets. These findings reveal toxicological mechanisms driving LUAD and offer potential therapeutic targets.
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