ArticleDrug design, development and therapy2024
Co-Expression Network Analysis and Molecular Docking Demonstrate That Diosgenin Inhibits Gastric Cancer Progression via SLC1A5/mTORC1 Pathway.
Article in Drug design, development and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Screening of core targets for Di(2-ethylhexyl) Phthalate-related gastric cancer based on machine learning, molecular docking, and SHAP analysis.PLoS computational biology · 2026Article
- Juglone targets CBS to inhibit the Wnt/β-catenin pathway and promotes osteosarcoma cell apoptosis.iScience · 2026Article
- Linalool targets NR3C2 to inhibit NF-κB-mediated gastric cancer progression.Cell division · 2026Article
- Therapeutic potential of diosgenin in hepatocellular carcinoma through molecular mechanisms and nanodelivery strategies.Discover oncology · 2026Review
- Role of diosgenin in gastrointestinal cancers: recent trends and future perspectives.Medical oncology (Northwood, London, England) · 2025Review
- Procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 discriminates AGS and MKN45 cells of human gastric cancer.Gastroenterology and hepatology from bed to bench · 2025Article
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Authors and funding
2 authors.
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Abstract
Background: Tumor-Node-Metastasis (TNM) stage of gastric cancer (GC) is one of the main factors affecting clinical outcome. The aim of this study was to explore the targets related to TNM stage of GC, and screening natural bioactive drug. Methods: RNA sequencing data of the TCGA-STAD cohort were downloaded from UCSC database. Genes associated with TNM staging were identified by weighted gene co-expression network analysis (WGCNA). Univariate Cox regression, least absolute shrinkage and selection operator (LASSO), extreme gradient boosting (Xgboost), random forest (RF) and cytohubba plug-in of cytoscope were applied to screen hub genes. Natural bioactive ingredients were available from the HERB database. Molecular docking was used to evaluate the binding activity of active ingredients to the hub protein. CCK-8, flow cytometry, transwell and Western blot assays were used to analyze the effects of diosgenin on GC cells. Results: 898 TNM-related genes were screened out through WGCNA. Three genes associated with GC progression/prognosis were identified, including nuclear receptor subfamily 3 group C member 2 (NR3C2), solute carrier family 1 member 5 (SLC1A5) and FAT atypical cadherin 1 (FAT1) based on the machine learning algorithms and hub co-expression network analysis. Diosgenin had good binding activity with SLC1A5. SLC1A5 was highly expressed in GC and was closely associated with tumor stage, overall survival and immune infiltration of GC patients. Diosgenin could inhibit cell viability and invasive ability, promote apoptosis and induce cell cycle arrest in G0/G1 phase. In addition, diosgenin promoted cleaved caspase 3 expression and inhibited Ki67, cyclin D1, p-S6K1, and SLC1A5 expression levels, while the mTORC1 activator (MHY1485) reversed this phenomenon. Conclusion: For the first time, this work reports diosgenin may inhibit the activation of mTORC1 signaling through targeting SLC1A5, thereby inhibiting the malignant behaviors of GC cells.
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