The inhibitory mechanism of compound K on A549 lung cancer cells through EGF pathway: an in silico and in vitro approach

被引:5
作者
Castro-Aceituno, Veronica [1 ]
Siddiqi, Muhammad Hanif [2 ,3 ]
Ahn, Sungeun [1 ]
Sathishkumar, Natarajan [2 ,3 ]
Noh, Hae Yong [1 ]
Simu, Shakina Yesmin [2 ,3 ]
Perez, Zuly E. Jimenez [2 ,3 ]
Yang, Deok Chun [1 ,2 ,3 ]
机构
[1] Kyung Hee Univ, Coll Life Sci, Dept Oriental Med Biotechnol, Yongin 446701, South Korea
[2] Kyung Hee Univ, Coll Life Sci, Grad Sch Biotechnol, Yongin 446701, South Korea
[3] Kyung Hee Univ, Coll Life Sci, Ginseng Bank, Yongin 446701, South Korea
来源
CURRENT SCIENCE | 2016年 / 111卷 / 06期
关键词
Epidermal growth factor; lung cancer; molecular docking simulation; Panax ginseng; TYROSINE KINASE INHIBITORS; GROWTH-FACTOR RECEPTOR; PANAX-GINSENG; BREAST-CANCER; THERAPY; GINSENOSIDES; APOPTOSIS;
D O I
10.18520/cs/v111/i6/1071-1077
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 anti-metastatic 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.
引用
收藏
页码:1071 / 1077
页数:7
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