ArticleFrontiers in public health2026
Multi-omics integration reveals inhibitory effects of carbon ion radiation on lung adenocarcinoma proliferation.
Article in Frontiers in public health, 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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Abstract
Objective: To analyze the inhibitory effect of carbon ion (C-ion) radiation-induced biological effects on the proliferation of lung adenocarcinoma (LUAD) by multi-omics integration. Methods: We investigated C-ion radiation effects on LUAD cellular responses using A549 and LLC cell lines. Clonogenic survival assays, DNA damage, and metastasis quantified radiation sensitivity, while a multi-cell co-culture system (A549/Beas-2B/LLC/MLE-12) differentiated direct vs. bystander effects. Integrated transcriptomics and targeted metabolomics identified radiation-responsive genes/metabolites, with pathway analysis conducted through MetaboAnalyst 6.0. Clinical relevance of CPT1, GCH1, and EPAS1 was assessed using UCSC Xena and Kaplan-Meier Plotter survival data. Radiation-induced molecular changes were validated by RT-qPCR and immunoblotting across cell types. An A549 tumor-bearing mouse model was established, and the growth and tumor size of the tumor-bearing mice were observed after irradiation with C-ions. Blood was taken from mice after anesthesia and necropsy to detect changes in the major differential metabolism factor arachidonic acid (AA), and tumor tissues were examined to detect changes in the expression of CPT1, GCH1, and EPAS1 in the tissues. Results: C-ion irradiation exerts a dual anti-proliferative effect on lung adenocarcinoma cells: it directly induces DNA damage (increased γ-H2AX/53BP1 foci), suppresses clonogenic survival, and inhibits tumor cell migration and invasion ( Conclusion: C-ion irradiation suppresses lung adenocarcinoma through a dual mechanism involving direct induction of cellular DNA damage and a metabolically enhanced bystander effect, driven by the CPT1/GCH1/EPAS1 regulatory axis, with arachidonic acid serving as a key downstream mediator.
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