Cucurbitacin IIb induces apoptosis and cell cycle arrest through regulating EGFR/MAPK pathway
文献类型： 外文期刊
作者： Liang, Yuan 1 ; Zhang, Tiehua 1 ; Ren, Li 1 ; Jing, Siyuan 1 ; Li, Zhuolin 2 ; Zuo, Peng 2 ; Li, Tiezhu 2 ; Wang, Yongjun 2 ;
作者机构： 1.Jilin Univ, Coll Food Sci & Engn, Changchun 130062, Peoples R China
2.Jilin Acad Agr Sci, Inst Agr Biotechnol, Changchun 130033, Peoples R China
关键词： Cucurbitacin IIb (CuIIb); Epidermal growth factor receptor (EGFR); Tyrosine kinase inhibitor (TKI); Apoptosis; Cell cycle arrest; Binding mode
期刊名称：ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY （ 影响因子：4.86； 五年影响因子：4.462 ）
ISSN： 1382-6689
年卷期： 2021 年 81 卷
页码：
收录情况： SCI
摘要： Epidermal growth factor receptor (EGFR) is considered as a valid target in the clinical trials of anticancer therapy and tyrosine kinase inhibitors (TKIs) of EGFR are approved for cancer treatments. In present work, cucurbitacin IIb (CuIIb) was confirmed to exhibit the proliferation inhibitory activity in A549 cells. CuIIb induced apoptosis via STAT3 pathway, which was mitochondria-mediated and caspase-dependent. CuIIb also suppressed the cell cycle and induced G2/M phase cell cycle arrest. CuIIb was capable of suppressing the signal transmitting of the EGFR/mitogen-activated protein kinase (MAPK) pathway which was responsible for the apoptosis and cell cycle arrest. Homogeneous time-resolved fluorescence (HTRF) analysis demonstrated that the kinase activity of EGFR was inhibited by CuIIb. Molecular docking suggested that the CuIIb-EGFR binding fundamentally depends on the contribution of both hydrophobic and hydrogen-bonding interactions. Hence CuIIb may serve as a potential EGFR TKI.
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