Wu Cunen, Zhuang Yuwen, Jiang Shan, Tian Fang, Teng Yuhao, Chen Xu, Zheng Peiqiu, Liu Shenlin, Zhou Jinyong, Wu Jian, Wang Ruiping, Zou Xi
The Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of TCM, Nanjing, Jiangsu 210029, China.
Division of Membrane Dynamics, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Int J Biochem Cell Biol. 2017 Mar;84:58-74. doi: 10.1016/j.biocel.2017.01.005. Epub 2017 Jan 16.
Cinnamaldehyde, the main chemical component of the essential oil separated from the traditional herb Cinnamomum cassia, has been demonstrated to be an efficient cytotoxic agent against several human cancers. The present experiment showed that cinnamaldehyde dose-dependently depresses the proliferation of three types of NSCLC cells and induces cell apoptosis in vitro and in vivo. Moreover, cinnamaldehyde attenuated CoCl-induced EMT and decreased matrix metalloprotease (MMP) family while the in vivo study showed the same trend. Mechanistically, cinnamaldehyde imitated the suppressive effect of XAV939 on cell motility and EMT which could be impaired by LiCl. Collectively, our research demonstrated for the first time that cinnamaldehyde is able to inhibit NSCLC cell growth by inducing apoptosis and reverse EMT through terminating Wnt/β-catenin pathway, which might supply further insight into cinnamaldehyde-mediated anti-tumor effect against NSCLC for better prognosis.
肉桂醛是从传统草药肉桂中分离出的精油的主要化学成分,已被证明是一种针对多种人类癌症的有效细胞毒性剂。本实验表明,肉桂醛在体外和体内均呈剂量依赖性地抑制三种非小细胞肺癌(NSCLC)细胞的增殖并诱导细胞凋亡。此外,肉桂醛减弱了氯化钴诱导的上皮-间质转化(EMT),并降低了基质金属蛋白酶(MMP)家族水平,而体内研究也显示出相同趋势。从机制上讲,肉桂醛模拟了XAV939对细胞运动性和EMT的抑制作用,而氯化锂可损害这种作用。总体而言,我们的研究首次证明,肉桂醛能够通过诱导凋亡来抑制NSCLC细胞生长,并通过终止Wnt/β-连环蛋白信号通路来逆转EMT,这可能为肉桂醛介导的针对NSCLC的抗肿瘤作用提供进一步的见解,以实现更好的预后。