ArticleScientific reports2026
Forsythiaside A inhibits progression and induces autophagy in lung adenocarcinoma: an integrated study combining network pharmacology and experimental validation.
Article in Scientific reports, 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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11 authors.
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Abstract
Lung adenocarcinoma (LUAD) is a lethal malignancy with limited treatment options, underscoring the need for novel agents. Forsythiaside A (FSA), a primary active component of Forsythia suspensa, possesses anti-inflammatory and antioxidant properties, but its role in lung adenocarcinoma remains unexplored. This study integrated network pharmacology, molecular docking, and experimental validation to investigate the anti-tumor effects of FSA and its underlying mechanism. Network analysis identified 218 potential targets, with enrichment in the PI3K-Akt signaling pathway. Molecular docking revealed a strong interaction between FSA and ESR1. Functionally, FSA potently inhibited the proliferation, migration, invasion, and colony formation of A549 and H1975 cells in vitro. This anti-tumor activity was confirmed in vivo in a mouse xenograft model. Mechanistically, FSA downregulated ESR1 expression, reduced phosphorylation of PI3K and AKT, and promoted autophagic flux, as evidenced by increased LC3-II/LC3-I ratio, decreased p62 expression, loss of mitochondrial membrane potential (JC-1), enhanced LC3 puncta formation, and ultrastructural changes consistent with autophagy. These findings indicate that FSA induces autophagy via the ESR1/PI3K/AKT axis and exhibits significant anti-tumor effects, highlighting its potential as a novel candidate for LUAD therapy.
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