Methylanthraquinone from Hedyotis diffusa WILLD induces Ca2+-mediated apoptosis in human breast cancer cells
Methylanthraquinone from Hedyotis diffusa WILLD induces Ca2+-mediated apoptosis in human breast cancer cells
复制标题
DOI：
10.1016/j.tiv.2009.08.002
复制
发表时间：
2010-02-01
影响因子：
3.2
通讯作者：
Li, Jianchun
中科院分区：
文献类型：
--
作者：
Liu, Zheng;Liu, Ming;Li, Jianchun
白花蛇舌草中的甲基蒽醌对多种肿瘤细胞具有较强的抗肿瘤活性。然而，甲基蒽醌诱导细胞凋亡的确切机制和信号通路尚未完全阐明。因此，我们探讨了甲基蒽醌介导MCF-7人乳腺癌细胞凋亡的机制。甲基蒽醌与MCF-7细胞共孵育后，凋亡细胞比例和细胞周期S期明显增加。此外，在MCF-7细胞暴露于甲基蒽醌后，细胞内钙水平升高，JNK磷酸化和钙蛋白酶激活。随着甲基蒽醌介导的线粒体膜电位的降低，细胞色素c从线粒体释放到胞质溶胶中。此外，甲基蒽醌强烈诱导MCF-7细胞中caspase-4、caspase-9和caspase-7的切割。结果提示白花蛇舌草中的甲基蒽醌通过Ca（2+）/calpain/caspase-4途径诱导MCF-7细胞凋亡。(C)2009年由Elsevier Ltd.出版
Methylanthraquinone from Hedyotis diffusa WILLD exhibited potent anticancer activity in many kinds of cancer cells. However, the exact mechanism and signaling pathway involved in methylanthraquinone-induced apoptosis have not been fully elucidated. Therefore, we explored the mechanisms of methylanthraquinone-mediated apoptosis in MCF-7 human breast cancer cells. When MCF-7 cells were co-incubated with methylanthraquinone, the percentage of apoptotic cell and S phase of cell cycle was markedly increased. In addition, a rise in intracellular calcium levels, phosphorylation of JNK and activation of calpain were found in MCF-7 cells after exposure to methylanthraquinone. With the methylanthraquinone-mediated reduction of mitochondrial membrane potential, cytochrome c was released from mitochondria to cytosol. Moreover, methylanthraquinone strongly induced cleavage of caspase-4, caspase-9 and caspase-7 in MCF-7 cells. These results suggested that methylanthraquinone from Hedyotis diffusa WILLD induced MCF-7 cells apoptosis via Ca(2+)/calpain/caspase-4 pathway. (C) 2009 Published by Elsevier Ltd.