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Fig. 3 | Journal of Hematology & Oncology

Fig. 3

From: Preclinical anti-myeloma activity of EDO-S101, a new bendamustine-derived molecule with added HDACi activity, through potent DNA damage induction and impairment of DNA repair

Fig. 3

EDO-S101 induces cell cycle arrest, apoptosis, and mitochondrial permeability deregulation. a Different MM cell lines were incubated with 1 and 2.5 μM EDO-S101. After propidium iodide (PI) staining, the cell cycle profile was analyzed by flow cytometry. b Annexin-V labeling of MM1S cells after treatment with different doses of EDO-S101 for 48 h and evaluated by flow cytometry. c Dose and time-response changes of proteins involved in apoptosis after EDO-S101 treatment of MM1S cells. d Effect of the pre-incubation for 24 h with the pan-caspase inhibitor Z-VAD-FMK (50 μM) on the apoptosis induced by EDO-S101 at 10 μM. Bortezomib 2 nM was used as a positive control of caspase dependent apoptosis. Data are presented as mean ± SD. e Changes in mitochondrial membrane potential after treatment with EDO-S101 as measured by flow cytometry with DioC6 staining. f Subcellular distribution of AIF in mitochondrial and nuclear fractions, in the MM1S cell line after EDO-S101 treatment

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