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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Inhibition of autophagy enhances the selective anti-cancer activity of tigecycline to overcome drug resistance in the treatment of chronic myeloid leukemia

Fig. 2

Tigecycline 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 < 0.05

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