Ginkgol C17:1 has been shown to inhibit apoptosis and migration of cancer cells,but the underlying mechanisms are not fully elucidated.In this study,we explored whether the inhibitory effects of Ginkgol C17:1 were associated with epidermal growth factor receptor(EGFR) and PI3K/Akt signaling.The results showed that EGF treatment increased the phosphorylation of EGFR,PI3 K,Akt,mTOR and NF-κB,and also enhanced the proliferation,migration and invasion of HepG2 cells.Ginkgol C17:1 dose-dependently inhibited EGF-induced phosphorylation/activation of all the key components including EGFR,PI3 K,Akt,mTOR and NF-kB,leading to a significant reduction either of proliferation or migration and invasion of HepG2 cells.Notably,treatment with Ginkgol C17:1 in mice suppressed the growth of tumor mass in vivo,and expression of EGFR in the tumor tissue.The results suggest that Ginkgol C17:1 is a potent tumor inhibiting compound that acts on EGF-induced signal transduction of the PI3K/Akt signaling pathways,and may represent a clinically interesting candidate for cancer therapy.
