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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

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

Fig. 4

Tigecycline causes apoptosis of CML cells by activating the cytochrome c/caspase-9/caspase-3 signaling pathway. (a) Apoptosis assay of the CML cells in response to stimulation with tigecycline. Left panel: a representative flow cytometry plots for CML cells stained with annexin V-FITC/PI-stained. Right panel: percentage apoptosis of the CML cells. Apoptosis was defined as the percentage of annexin V-positive cells. (b) Western blot analyses of cytochrome c, cleaved caspase-9, and caspase-3 protein levels. Cyto.C (Mito), cytochrome c protein in the mitochondria; Cyto.C (Cyto), cytochrome c protein in the cytoplasm. Cytochrome c oxidase-4 and β-actin were used as the reference proteins for the analyses of mitochondrial and cytoplasmic proteins, respectively. *P < 0.05

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