ArticleFrontiers in pharmacology2025
Eupalinolide A inhibits cancer progression and induces ferroptosis and apoptosis by targeting the AMPK/mTOR/SCD1 signalling in non-small cell lung cancer.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- KNL1 Regulates Ferroptosis Resistance and Migration in Lung Adenocarcinoma Cells via AMPK-mTOR Signaling.Oncology research · 2026Article
- Pemetrexed sensitizes cisplatin therapy by inducing ferroptosis in NSCLC cells.Frontiers in pharmacology · 2025Article
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19 authors.
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Abstract
Background: Non-small cell lung cancer (NSCLC) is a common malignancy with limited efficacy of established therapies and a poor prognosis that often entails a high financial burden. Eupatorium lindleyanum DC. and its main component Eupalinolide A (EA) are clinically used for the management of chronic tracheitis. Therefore, the aim of this study was to investigate the effects of EA on NSCLC and its underlying molecular mechanisms. Methods: The effect of EA was assessed on A549 and H1299 tumour cells by flow cytometry, qRT-PCR, western blotting, TUNEL assay, molecular docking, RNA sequencing, non-target metabolomics experimental methodology, and phosphoproteomics to explore the molecular pathways and specific targets. A mouse tumour xenograft model was used to evaluate its effect Results: EA inhibited cell proliferation by arresting the cell cycle at the G2/M phase (increasing the proportion of G2-phase cells in A549 cells from 2.91% to 21.99% and their proportion in H1299 cells from 8.22% to 18.91%). It also promoted apoptosis (increasing the total apoptotic rate in A549 cells from 1.79% to 47.29% and that in H1299 cells from 4.66% to 44.43%) as well as ferroptosis (increasing ROS production by 2.46-fold in A549 cells and by 1.32-fold in H1299 cells). This mechanism was mediated by the modulation of the synthesis of unsaturated fatty acids through the downregulation of stearoyl-CoA desaturase 1 (SCD1) expression, which was reduced by 34% in A549 cells and by 48% in H1299 cells. Notably, the supplementation of oleic acid counteracted the inhibitory effect of EA on cell proliferation and migration. These effects of EA were due to the involvement of the AMPK- mTOR signalling pathway. EA treatment (25 mg/kg) markedly inhibited tumour growth Conclusion: EA inhibited the proliferation and migration of NSCLC cells by the modulation of lipid metabolism through the activation of the ROS-AMPK-mTOR-SCD1 signalling pathway. Therefore, EA might be considered as a promising candidate in the development of therapeutics against NSCLC.
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