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<p>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.</p>

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Forsythiaside A inhibits progression and induces autophagy in lung adenocarcinoma: an integrated study combining network pharmacology and experimental validation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月13日

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  • Xiaoxiao Yin,
  • Shiyi Li,
  • Hongli Li,
  • Zihan Kong,
  • Yanan Du,
  • Yanjing Dong,
  • Shunfu Hou,
  • Xiuying Gong,
  • Yong Li,
  • Haixia Wang,
  • Chonggao Yin

摘要

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.