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. 2019 Aug 13;10(8):617. doi: 10.1038/s41419-019-1851-3

Fig. 2. AML-derived cells are more sensitive to mitocan treatment.

Fig. 2

a Relative mtDNA content before and after 24 h exposure to doxorubicin treatment in AML cell lines (left) or in solid tumor cell lines (right). b Correlation between basal mtDNA content and LD50 of mitocans. Normalization of LD50 values was performed using min-max approach, linear functions were adjusted for the data using lm() method in R. Basal ATP level (c) and ATP-linked respiration (d) before and after exposure to doxorubicin for 24 h (c) or 4 h (d). e ATP synthase β subunit protein level before and after 24 h exposure to doxorubicin. β-actin was used as a loading control. f Changes in mitochondrial mass after 24 h doxorubicin treatment. Comparison of MOLM-13 vs. normal PBMCs is shown. g Mitochondrial membrane potential before and after 4 h doxorubicin treatment, as defined by JC-1 staining. Representative plots for red/green fluorescence (PE vs. FITC) after standard compensation for MOLM-13, healthy PBMCs, and SKOV3 cells are shown below for the untreated (blue) and doxorubicin-treated (red) cells. h Expression ratios of mitochondrial fusion/fission genes before and after 8 h doxorubicin treatment. The results of 3–6 independent experiments are presented as mean ± SD (in a, c, f, g, h) or mean ± SEM (in d, e). All technical replicates are shown in c. For statistical significance, either Student’s t-test with independent samples (a, c, eh) or ANOVA with subsequent Dunn’s test (d) was used. ***p < 0.001; **p < 0.01; *p < 0.05; ns: p > 0.05