Tunicamycin promotes apoptosis in leukemia cells through ROS generation and downregulation of survivin expression

摘要: Tunicamycin (TN), one of the endoplasmic reticulum stress inducers, has been reported to inhibit tumor cell growth and exhibit anticarcinogenic activity. However, mechanism by which TN initiates apoptosis remains poorly understood. In present study, we investigated effect on apoptotic pathway in U937 cells. We show that induces association with caspase-3 activation, generation reactive oxygen species (ROS), downregulation survivin expression. P38 MAPK (mitogen-activated protein kinase) ROS signaling play crucial roles TN-induced hypothesized activation p38 is responsible for death. To test this hypothesis, selectively inhibited during treatment TN. Our data demonstrated inhibitor (SB), but not ERK (PD) or JNK (SP), partially maintained Pre-treatment NAC GSH markedly prevented death, suggesting a role process. Ectopic expression cells attenuated suppression cleavage, mitochondrial membrane potential, cytochrome c release Taken together, our results modulates multiple components response human leukemia raise possibility novel therapeutic strategy hematological malignancies.