Fig. 2From: Inhibition of autophagy enhances the selective anti-cancer activity of tigecycline to overcome drug resistance in the treatment of chronic myeloid leukemiaTigecycline suppresses mitochondrial biogenesis in CML cell lines and primary cells. (a) Effects of increasing concentrations of tigecycline on the protein levels of cytochrome c oxidase (Cox)-1, Cox-2, and Cox-4 in CML cell lines and primary cells. Tubulin was used as the reference protein in the western blotting. All the cells were cultured with tigecycline for 48 h before the experiments were conducted. (b) The relative mRNA levels of Cox-1, Cox-2, and Cox-4 in CML cells after treatment with tigecycline. (c) Evaluation of the mitochondrial membrane potential of tigecycline-treated CML cells using JC-1 staining and flow cytometry. Carbonyl cyanide 3-chlorophenylhydrazone (CCCP) was used as the positive control. (d) Reactive oxygen species (ROS) levels in the CML cells were measured by flow cytometry. Ctrl, control; TI, tigecycline-treated cells. *P < 0.05Back to article page