Conclusion
DET inhibits GBM cell invasion, proliferation, and apoptosis via modulating the PI3K/AKT signaling pathway, highlighting its potential as a novel therapeutic strategy for GBM treatment.
Methods
Using PharmMapper, the chemical structure of DET was examined for possible targets after being acquired from PubChem. GBM-related targets were obtained through multi-omics approaches. A protein-protein interaction (PPI) network was constructed using Cytoscape and STRING, and target binding was evaluated through molecular docking. Enrichment analysis was conducted using Metascape. The effects of DET on GBM cell invasion, apoptosis, and proliferation were assessed through in vitro assays, including Transwell, EDU, CCK8, and flow cytometry. Western blot analysis was performed to examine the components of the PI3K/AKT signaling pathway.
Results
Among the sixty-four shared targets identified, JUN and CCND1 were the most frequently observed. Enrichment analysis demonstrated that DET influenced the MAPK and PI3K/AKT signaling pathways. In Transwell assays, DET significantly inhibited the invasive behavior of glioma cells. Western blot analysis further confirmed the downregulation of EGFR, JUN, and PI3K/AKT.