The Mechanism of Scopolamine’s Effect on Migration Function of Lung Cancer Cells: A Network Pharmacology and Bioinformatics Perspective

Abstract

Background. This study utilized network pharmacology and bioinformatics analysis to identify the hub genes influenced by scopolamine in lung cancer. Methods. The effect of scopolamine on lung cancer was investigated by cell invasion assay and cell scratch assay. The analysis involved protein-protein interaction (PPI) networks topology analysis to identify these genes, and subsequent differential analysis and survival analysis were conducted using gene expression profile interaction analysis (GEPIA). Furthermore, the findings were supported by molecular docking experiments for verification. Results. Results from cell invasion and scratch assays suggest that scopolamine inhibits the migration of lung cancer cells. JAK2, JAK3, CCR5, and ACE were identified as the top four hub genes that have an impact on lung cancer. KEGG enrichment analysis revealed that the scopolamine response in lung cancer is significantly associated with ten pathways, including “neuroactive ligand-receptor interaction in cancer,” “PD-1 checkpoint pathway in cancer,” “chemokine signaling pathway,” “PD-L1 expression,” and others. Additionally, the expression levels of JAK2, JAK3, CCR5, and ACE were found to be correlated with survival in patients with lung cancer. Furthermore, molecular docking experiments demonstrated that scopolamine binds and forms stable complexes with the protein products of all four aforementioned genes. The main targets of scopolamine in the treatment of lung cancer are JAK2, JAK3, CCR5, and ACE. Conclusion. Scopolamine has a significant effect on various cellular functions in lung cancer cells, potentially reducing the likelihood of metastasis. Based on these findings, it is recommended to consider administering scopolamine as part of the preoperative phase for patients with lung cancer.