Department of Animal Science, School of Life Sciences, Bharathidasan University, Tiruchirappalli, 620 024, Tamil Nadu, India.
Biotechnol Lett. 2013 Sep;35(9):1395-403. doi: 10.1007/s10529-013-1238-y. Epub 2013 May 21.
Verrucarin A (VA), a protein synthesis inhibitor, derived from the pathogen fungus Myrothecium verrucaria, inhibits growth of leukemia cell lines and activates caspases and apoptosis and inflammatory signaling in macrophages. We have investigated VA-induced growth inhibition in breast cancer cells MDA-MB-231 and T47D and, particularly, the mechanism of VA-induced apoptosis. VA treatment brought about apoptotic cell death in a dose- and time-dependent manner which was associated with chromatin condensation, cell shrinkage, nuclear fragmentation and intracellular ROS production. Mitochondrial membrane depolarization, activation of caspase-3, down-regulation of Bcl-2 expression and up-regulation of Bax and p53 expression were observed. VA thus affects the viability of both the breast cancer cells by triggering ROS-mediated intrinsic mechanism of apoptosis.
疣孢漆斑菌 A（VA）是一种蛋白合成抑制剂，来源于病原菌漆斑菌，它可以抑制白血病细胞系的生长，并激活巨噬细胞中的胱天蛋白酶和细胞凋亡及炎症信号。我们研究了 VA 对乳腺癌细胞 MDA-MB-231 和 T47D 的生长抑制作用，特别是 VA 诱导细胞凋亡的机制。VA 处理以剂量和时间依赖的方式引起细胞凋亡死亡，与染色质浓缩、细胞收缩、核片段化和细胞内 ROS 产生有关。观察到线粒体膜去极化、 caspase-3 的激活、Bcl-2 表达下调以及 Bax 和 p53 表达上调。因此，VA 通过触发 ROS 介导的内在细胞凋亡机制影响两种乳腺癌细胞的活力。
