The mechanism of total ginseng extracts in the treatment of lung cancer progression based on network pharmacology and experimental validation

Abstract

Objective: The objective of this study was to investigate the mechanism by which total ginseng extract (TGE) inhibits the progression of lung cancer through network pharmacology and experimentation. Materials and Methods: A Lewis lung carcinomas (LLC) model was established by injecting cancer cells through the tail vein and through administering different doses of TGE. The infiltrated immune cells into the microenvironment of lung cancer metastasis through flow cytometry were evaluated, and the messenger RNA (mRNA) expression levels of various immune cell-related chemokines were determined using quantitative reverse transcription–polymerase chain reaction. Therapeutic targets and signaling pathways of TGE in nonsmall cell lung cancer were investigated using systematic pharmacology and virtual docking. Immunoblotting was performed to determine the impacts of TGE on migration-related proteins. Results: Flow cytometry showed that 1.82 g/kg TGE increased the infiltrated T cells and inhibited the recruitment of myeloid cells, which was caused by decreased mRNA expression of chemokines after TGE treatment. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses showed that the delayed progression of lung cancer by TGE might be related to the promotion of lung cancer cell apoptosis-associated signaling pathways. The virtual docking results indicated that the active components of ginseng are directly bound to apoptosis-related proteins. Immunoblotting showed that TGE inhibited tumor metastasis by regulating the expression of migration-related proteins. Conclusions: The study reveals the potential mechanism of ginseng extract in the treatment of lung cancer progression and provides a reliable basis for its clinical application.