Pelargonidin inhibits vascularization and metastasis of brain gliomas by blocking the PI3K/AKT/mTOR pathway

Pelargonidin has attracted much attention in many cancers. Whether the growth of glioma inhibited by pelargonidin is related to the PI3K/AKT/mTOR pathway is unknown. To examine this, we performed both in vivo and in vitro studies. Twenty-four hours after inoculation, C6 cells received various treatments: CCK8, transwell, flow cytometry, and Western blot were performed. The cell supernatant was collected in order to pretreat HUVEC cells, and tube formation assay was performed. An in situ glioma rat model was constructed and administrated treatment according to its group. After 14 days, the brains were obtained for TUNEL assay, immunohistochemical staining, and Western blot. In vitro studies demonstrated that pelargonidin inhibited the proliferation, migration, and invasion of C6 cells, and promoted apoptosis of C6 cells. Additionally, pelargonidin could inhibit tube formation of HUVECs. We also detected the proteins in the PI3K/AKT/mTOR pathway, and the results indicated that pelargonidin inhibited the phosphorylation of AKT, PI3K, and mTOR, and downregulated VEGF protein. In vivo glioma models were successfully built, and pelargonidin could increase the survival rate of rat, and pathological staining results indicated that pelargonidin increased TUNELpositive cells and decreased micro-vessel density (MVD) through PI3K/AKT/mTOR. Pelargonidin could reduce the relative expression of MMP2, MMP9, N-cadherin, and VEGF proteins, and inhibit the PI3K/AKT/ mTOR pathway. Pelargonidin inhibited the vascularization and metastasis of glioma by blocking the PI3K/ AKT/mTOR pathway.