In previous studies compound K (CK), an active metabolite ginsenoside from Panax ginseng, was shown to exhibit anti-cancer activity. However, the mechanism of CK through the EGFR/H-Ras pathway in cancer cells has not been reported so far. Therefore, we focused on the effect of CK as an EGFR and H-Ras inhibitor by in silico and in vitro studies using A549 cells. The biological activity prediction shows that CK exhibits chemopreventive, anticarcinogenic and antimetastatic activity. Also, using molecular docking studies it has been shown that CK exhibits a strong binding energy with EGFR and H-Ras than Erlotinib. CK inhibits cell viability, decreases cell migration, induces apoptosis and strongly decreases gene expression of EGFR and H-Ras genes in vitro. This finding suggests that the EGFR pathway is involved in the anti-cancer activity of CK of EGF-enhanced A549 lung cancer cell line.
Keywords
Epidermal Growth Factor, Lung Cancer, Molecular Docking Simulation, Panax ginseng,/i>.
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