ArticleFrontiers in pharmacology2026
Integrating multi-omics approaches reveals metabolic reprogramming and identifies PDHX as a candidate node in triptolide-treated non-small Cell lung cancer.
Article in Frontiers in pharmacology, 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
Introduction: Metabolic reprogramming is a central driver of malignant progression in non-small cell lung cancer (NSCLC). However, conventional targeted therapies face significant limitations due to drug resistance and narrow therapeutic windows. Triptolide, a natural tricyclic diterpenoid derived from Tripterygium wilfordii, exhibits potent antitumor activity, yet its precise mechanisms for modulating metabolic reprogramming in NSCLC remain elusive. Methods: Using NSCLC cell models, we assessed TPL effects on proliferation, migration, and mitochondrial function Results: TPL significantly inhibited NSCLC cell proliferation and induced metabolic alterations characterized by glycolytic suppression (HK2 downregulation) and concurrent disruption of mitochondrial oxidative phosphorylation (OXPHOS)-associated proteins. Metabolomics revealed systemic metabolic shifts, with pyruvate metabolism and glutathione pathways being most significantly altered. Mechanistically, multi-omics analysis identified PDHX as a key node within a broader metabolic network disrupted by TPL, associated with glycolytic suppression ( Conclusion: These findings suggest that TPL exerts antitumor effects in NSCLC by disrupting both glycolysis and mitochondrial function, with PDHX identified as a candidate mediator. Further studies are warranted to explore its therapeutic potential.
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