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Yueying Li,Jun Liu,Xiaoming Yang,Yan Dong,Yali Liu,Min Chen.Journal of Biomedical Research,2017,31(3):232-239
Ginkgol C17:1 inhibits tumor growth by blunting the EGF-PI3K/Akt signaling pathway
Received:March 21, 2016  Revised:April 28, 2016
DOI10.7555/JBR.31.20160039
KeywordsGinkgol C17:1, epidermal growth factor, PI3K/Akt, HepG2
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AuthorInstitution
Yueying Li School of Medicine, Institute of Life Sciences
Jun Liu Institute of Life Sciences
Xiaoming Yang School of Food and Biological Engineering, Jiangsu University, Zhenjiang, Jiangsu , China
Yan Dong School of Medicine
Yali Liu School of Food and Biological Engineering, Jiangsu University, Zhenjiang, Jiangsu , China
Min Chen School of Medicine
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Abstract
      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, PI3K, Akt, mTOR and NF-kB, 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-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/vjjhhAkt signaling pathways, and may represent a clinically interesting candidate for cancer therapy.
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