20(S)-Ginsenoside Rg3 Inhibits Lung Cancer Cell Proliferation by Targeting EGFR-Mediated Ras/Raf/MEK/ERK Pathway

文献类型： 外文期刊

第一作者： Liang, Yuan

作者： Liang, Yuan;Zhang, Tiehua;Jing, Siyuan;Zhang, Jie;Zuo, Peng;Li, Tiezhu;Wang, Yongjun;Xing, Shaochen;Wei, Zhengyi

作者机构：

关键词： Epidermal Growth Factor Receptor; 20(S)-Ginsenoside Rg3; Cell Proliferation; Cell Cycle; Binding Interaction

期刊名称：AMERICAN JOURNAL OF CHINESE MEDICINE （ 影响因子：3.682； 五年影响因子：3.22 ）

ISSN： 0192-415X

年卷期： 2021 年 49 卷 03 期

页码：

收录情况： SCI

摘要： Lung cancer is the leading cause of cancer death in the world and classified into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). As tyrosine kinase inhibitors (TKIs), several triterpenoid saponins can target to epidermal growth factor receptor (EGFR), a widely used molecular therapeutic target, to exhibit remarkable anti-proliferative activities in cancer cells. As one of triterpenoid saponins, 20(S)-ginsenoside Rg3 [20(S)-Rg3] was confirmed to be an EGFR-TKI in this work. According to the quantitative real-time reverse transcription-PCR (qRT-PCR) and immunoblotting analysis, 20(S)-Rg3 was certified to play a key role on EGFR/Ras/Raf/MEK/ERK signal pathway regulation. Our data demonstrated that 20(S)-Rg3 might block the cell cycle at the G0/G1 phase by downregulating CDK2, Cyclin A2, and Cyclin E1. Molecular docking suggested that the combination of both hydrophobic and hydrogen-bonding interactions may help stabilizing the 20(S)-Rg3-EGFR binding. Furthermore, their binding stability was assessed by molecular dynamics simulation. Taken together, these data provide the evidence that 20(S)-Rg3 could prohibit A549 cell proliferation, probably by arresting the cell cycle at the G0/G1 phase via the EGFR/Ras/Raf/MEK/ERK pathway.

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