Ginkgol C17:1 inhibits tumor growth by blunting the EGF-PI3K/Akt signaling pathway
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 resu...
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Published in | Journal of biomedical research Vol. 31; no. 3; pp. 232 - 239 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
China
Editorial Department of Journal of Biomedical Research
01.01.2017
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | 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. 32-1810/R Ginkgol C17:1, epidermal growth factor, PI3K/Akt, HepG2 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 The authors reported no conflict of interests. |
ISSN: | 1674-8301 2352-4685 |
DOI: | 10.7555/JBR.31.20160039 |