Study Of Oscc Transition Via Network Pharmacology And Molecular Docking

To investigate the biological process underlying the progression of oral submucosal fibrosis (OSF) into oral squamous cell carcinoma (OSCC) induced by Areca catechu L. (AC) and to identify potential biomarkers and therapeutic targets for precision medicine. Pathogenic genes were extracted from GeneCards, OMIM, and DisGENET databases, while AC active ingredient targets were obtained from TCMSP and Batman-TCM databases. Interaction network was constructed to identify core targets, followed by GO and KEGG enrichment analyses to explore potential biological pathways. AlphaFold 3 was utilized to predict the structure of key target proteins, and AutoDock Vina was applied to evaluate the binding affinity between the AC active compound and key target proteins. Furthermore, Hematoxylin-eosin staining was conducted to observe pathological changes in OSF and OSCC tissues, and protein expression levels were verified using Western blotting. The study identified 24 AC compounds linked to 101 key targets in OSF-OSCC progression, revealing the PI3K/Akt signaling pathway as a central regulator among 28 enriched pathways through GO/KEGG analyses. Molecular docking further demonstrated a strong binding affinity between Dibutyl Phthalate and AKT1, supporting its potential role in OSCC progression. Western blot analysis confirmed significantly elevated PI3K and Akt expression in OSF-to-OSCC cases (P < 0.05). The PI3K/Akt pathway is central to OSF transformation into OSCC. Targeting Dibutyl Phthalate’s interaction with AKT1 within this pathway offers a novel strategy for early intervention and precision medicine in OSCC management.