Ginkgol C17∶1 inhibits tumor growth by blunting the EGF-PI3K/Akt signaling pathway
Yueying Li
Jun Liu
Xiaoming Yang
Yan Dong
Yali Liu
Min Chen
摘要：Ginkgol C 17∶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,PI3K,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,PI3K,Akt,mTOR and NF-κB,leading to a significant reduction either of proliferation or migration and invasion of HepG2 cells.Notably,treatment with Ginkgol C 17∶1 in mice suppressed the growth of tumor mass in vivo,and expression of EGFR in the tumor tissue.The results suggest that Ginkgol C 17∶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.
机标关键词：tumor growthgrowth factor receptorsignal transductioninhibitory effectscancer therapythe growth
分类号：R730.52(一般性问题)
资助基金：This study was supported by the National Natural Science Foundation of China(grant no.81372404)the Postdoctoral Foundation of China (grant no.2012M521018)the Zhenjiang Social Development Project (No.SH2015072)
论文发表日期：2017-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：8( 232-239 )
英文信息