Securinine Inhibits Glioblastoma Growth via the PI3K/AKT/mTOR Signaling Pathway

Objective To investigate the mechanism by which securinine inhibits glioblastoma (GBM) growth through the mTOR pathway and its potential application value in promoting GBM apoptosis. Methods GBM-related target genes and securinine-related target genes were obtained via network pharmacology analysis. In vitro cell experiments (using GBM cell lines treated with securinine to detect cell proliferation, apoptosis, and expression of PI3K/AKT/mTOR pathway-related proteins) and in vivo animal experiments (establishing GBM xenograft models to observe tumor growth and related molecular changes after securinine administration) were performed. Results In vitro experiments showed that securinine significantly inhibited GBM cell proliferation, induced apoptosis, reduced the phosphorylation levels of mTOR and its upstream key substrate proteins (e.g., PI3K, AKT), and suppressed pathway activity. In vivo experiments demonstrated that securinine effectively slowed tumor growth and prolonged the survival of tumor-bearing animals. Conclusion Securinine inhibits GBM growth through the mTOR pathway, providing strong evidence for its application in GBM treatment. It is expected to facilitate the development of novel securinine-based therapeutic strategies to improve the poor prognosis of GBM patients.