School of Life Sciences and Biopharmaceuticals, Shenyang Pharmaceutical University, Shenyang, China.
Toxicol In Vitro. 2010 Feb;24(1):142-7. doi: 10.1016/j.tiv.2009.08.002. Epub 2009 Aug 15.
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.
鸡矢藤中的甲基蒽醌在多种癌细胞中表现出很强的抗癌活性。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的 MCF-7 人乳腺癌细胞凋亡的机制。当 MCF-7 细胞与甲基蒽醌共同孵育时，细胞凋亡的比例和细胞周期的 S 期明显增加。此外，在 MCF-7 细胞暴露于甲基蒽醌后，发现细胞内钙离子水平升高，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降低，细胞色素 c 从线粒体释放到细胞质。此外，甲基蒽醌强烈诱导 MCF-7 细胞中 caspase-4、caspase-9 和 caspase-7 的裂解。这些结果表明，鸡矢藤中的甲基蒽醌通过 Ca(2+)/钙蛋白酶/caspase-4 途径诱导 MCF-7 细胞凋亡。
