Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Jan 19;31(3):232-239.
doi: 10.7555/JBR.31.20160039.

Ginkgol C17:1 inhibits tumor growth by blunting the EGF- PI3K/Akt signaling pathway

Yueying Li  1 , Jun Liu  2 , Xiaoming Yang  3 , Yan Dong  4 , Yali Liu  3 , Min Chen  4
Affiliations

Ginkgol C17:1 inhibits tumor growth by blunting the EGF- PI3K/Akt signaling pathway

Yueying Li et al. J Biomed Res. .

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 massin 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.

PubMed Disclaimer

Conflict of interest statement

The authors reported no conflict of interests.

Figures

Fig.1
Fig.1
Ginkgol C17:1 inhibits EGF-induced phosphorylation of EGFR in HepG2 cells.
Fig.2
Fig.2
Ginkgol C17:1 inhibits EGF-induced PI3k/Akt signaling activities.
Fig.3
Fig.3
Ginkgol C17:1 inhibits EGF-induced cell proliferation, migration and invasion.
Fig.4
Fig.4
The size of tumor mass and the immunestaining of EGFR inside the tumor tissue.
See this image and copyright information in PMC

References

    1. Prigent SA, Lemoine NR. The type 1 (EGFR-related) family of growth factor receptors and their ligands[J]. Prog Growth Factor Res, 1992, 4(1): 1–24. - PubMed
    1. Normanno N, Bianco C, De Luca A, et al. Target-based agents against ErbB receptors and their ligands: a novel approach to cancer treatment[J]. Endocr Relat Cancer, 2003, 10(1): 1–21. - PubMed
    1. Hynes NE, MacDonald G. ErbB receptors and signaling pathways in cancer[J]. Curr Opin Cell Biol, 2009, 21(2): 177–184. - PubMed
    1. Sharma SV, Bell DW, Settleman J, et al. Epidermal growth factor receptor mutations in lung cancer[J]. Nat Rev Cancer, 2007, 7(3): 169–181. - PubMed
    1. Boonsai P, Phuwapraisirisan P, Chanchao C. Antibacterial activity of a cardanol from Thai Apis mellifera propolis[J]. Int J Med Sci, 2014, 11(4): 327–336. - PMC - PubMed

LinkOut - more resources