ReferenceID 5129
The mechanism of dioscin preventing lung cancer based on network pharmacology and experimental validation
J Ethnopharmacol
Ethnopharmacological relevance: Dioscorea nipponica Makino as a Chinese folk medicine has been used for the treatment of chronic bronchitis, cough, and asthma. Several studies have established the antimetastatic potentia
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- Reference Id
- 5129
- Evidence Id
- 21719
- Core Evidence Id
- 21719
- Source Reference Id
- 3540
- Herb2 Reference Id
- HBREF004337
- Subject Paper Key
- HBIN024134_35245631
- Pubmed Id
- 35245631
- Doi
- 10.1016/j.jep.2022.115138
- Paper Title
- The mechanism of dioscin preventing lung cancer based on network pharmacology and experimental validation
- Paper Abstract
- Ethnopharmacological relevance: Dioscorea nipponica Makino as a Chinese folk medicine has been used for the treatment of chronic bronchitis, cough, and asthma. Several studies have established the antimetastatic potential of Dioscorea nipponica Makino extract. Dioscin is a major bioactive compound in Dioscorea nipponica Makino and has anti-tumor property in lung cancer cell lines. However, the preventive effect of dioscin against lung cancer and its key mechanism haven't been identified yet. Aim of study: To identify the prevention effect of dioscin on lung cancer and explore its key mechanism based on network pharmacology and experimental validation. Methods: The potential targets of dioscin were obtained from the HERB database. The therapeutic targets of lung cancer were acquired from the GeneCards database. Protein-protein interaction network (PPI) was constructed in the STRING 11.0 database. The David database was used for enrichment analysis. Molecular Docking was finished by the AutoDock Vina. NSCLC cell lines and mouse lung cancer model were used to confirm the prevention effect of dioscin on lung cancer and its key mechanism. Results: 76 potential targets of dioscin were identified to be involved in lung cancer treatment, which refer to 512 biological processes, 47 molecular functions, 77 cellular components and 107 signal pathways. The molecular docking suggested that dioscin might bind to AKT1, Caspase3, TP53, C-JUN and IL-6. The DARTS indicated that dioscin could bind to AKT1. In vitro, dioscin could decrease proliferation, invasion and migration in A549 and PC-9 cells with the significant reduction in the expression of p-AKT, MMP2, and PCNA. In vivo, dioscin could reduce lung nodules, lung injury, and mortality in mouse lung cancer model with reducing the expression of p-AKT, MMP2, PCNA and increasing the expression of active-caspase3. Conclusion: Dioscin could prevent lung cancer and its key target is AKT1 kinase, a center protein of PI3K/AKT signaling pathway.
- Journal
- J Ethnopharmacol
- Publish Year
- 2022
- Experiment Subject
- mouse; lung cancer cell lines; nsclc cell lines; pc-9 cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Chronic Bronchitis; Lung Nodules; Asthma; Cough; Lung Cancer; Lung Injury
- Paper Title Cn
- Paper Title En
- The mechanism of dioscin preventing lung cancer based on network pharmacology and experimental validation
- Bilingual Status
- semi_complete