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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Super-enhancer profiling identifies novel critical and targetable cancer survival gene LYL1 in pediatric acute myeloid leukemia

Fig. 3

GNE-987 restained the proliferation of AML cell lines. A drug sensitivity assay of NB4, Kasumi-1, HL-60, and MV4–11 cell lines after treatment with gradient concentrations of GEN987 for 24 h. B GNE-987 blocked cell cycle of AML cells. Cell cycle of NB4, Kasumi-1, HL-60, and MV4–11 cell lines were analyzed after treatment with DMSO or GNE-987 for 24 h. AML cells were distributed in G1/S phase and the cell population in G1 phase increased dramatically after treatment with GNE-987. C Annexin V and PI-labeled cell apoptosis of NB4 cell line analyzed by flow cytometry after DMSO or GNE-987 treatment for 24 h. The apoptotic rates of NB4 cell line were significantly increased after GNE-987 treatment. D Annexin V and PI-labeled cell apoptosis of Kasumi-1 cell line analyzed by flow cytometry after DMSO or GNE-987 treatment for 24 h. The apoptotic rates of Kasumi-1 cell line were significantly increased after GNE-987 treatment. E Annexin V and PI-labeled cell apoptosis of HL-60 cell line analyzed by flow cytometry after DMSO or GNE-987 treatment for 24 h. The apoptotic rates of HL-60 cell line were significantly increased after GNE-987 treatment. F Annexin V and PI-labeled cell apoptosis of MV4–11 cell line analyzed by flow cytometry after DMSO or GNE-987 treatment for 24 h. The apoptotic rates of MV4–11 cell line were significantly increased after GNE-987 treatment. G GNE-987 evicts BET protein expression in AML cells. Western blotting analysis showed that GNE-987 induced BET proteins degradation in NB4, Kasumi-1, HL-60, and MV4–11 cell lines. PARP was increased in NB4, Kasumi-1, HL-60, and MV4–11 cell lines with GNE-987 concentration-dependent manner

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