Stigmasterol inhibits the progression of hepatocellular carcinoma by modulating the TLR4/MyD88/NF-κB signaling pathway

Abstract

Purpose This study employs molecular docking and in vitro experiments to investigate the regulatory mechanism of stigmasterol on the TLR4/MyD88/NF-κB signaling pathway in hepatocellular carcinoma. Methods Molecular docking with the AutoDock program investigated stigmasterol's binding affinity with TLR4, MyD88, and NF-κB. Its impact on proliferation and migration was assessed via CCK8, wound healing, and Transwell assays, while clonogenicity was determined through clonogenic formation experiments. Apoptosis and cell cycle were examined using flow cytometry. Western blot analysis evaluated TLR4, MyD88, and NF-κB protein expression post-stigmasterol treatment Results Molecular docking revealed favorable binding conformations of stigmasterol with TLR4, MyD88, and NF-κB. stigmasterol exhibited inhibitory effects on proliferation, migration, invasion, and clonogenicity of hepatocellular carcinoma cells in vitro. Additionally, it promoted apoptosis, suppressed the cell cycle, and reduced the protein expression of the TLR4/MyD88/NF-κB signaling pathway. Conclusion stigmasterol suppresses the activity of hepatocellular carcinoma cells by modulating the TLR4/MyD88/NF-κB signaling pathway.