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Fig. 1 | Cancer Cell International

Fig. 1

From: GNF-7, a novel FLT3 inhibitor, overcomes drug resistance for the treatment of FLT3‑ITD acute myeloid leukemia

Fig. 1

GNF-7 potently inhibited the proliferation of FLT3-ITD AML cells and targeted FLT3-ITD downstream signaling pathways. A AML cell line MOLM-13, MV4-11, U937 and THP-1 were treated with DMSO or increasing concentrations of GNF-7 for 48 h and the normalized cell proliferation was measured by CellTiter Glo assay. B Mononuclear cells isolated from umbilical cord blood (Normal #1, Normal #2), bone marrow of diagnosed with AML (AML #1, AML #2) and AML harboring FLT3-ITD mutation (AML #3, AML #4, AML #5) were treated with different concentrations of GNF-7 for 48 h, and normalized cell proliferation was detected by CellTiter Glo assay. C Primary bone marrow cells isolated from AML #3 and AML #4 were exposed to GNF-7 for 4 h and then detected by western blotting with antibodies against phosphorylated and total of FLT3, Stat5, AKT and ERK, respectively. D Phosphorylated and total of FLT3, Stat5, AKT and ERK in MOLM-13 and MV4-11 cells treated with GNF-7 for 4 h were detected by western blotting. E Dose response curve of GNF-7 on Ba/F3 FLT3-ITD cells in the presence or absence of IL-3. F Ba/F3 FLT3-ITD cells were treated with the different concentration of GNF-7 for 4 h and subjected to western blotting with the indicated antibodies. All experiments were repeated three times with the same results. Data are presented as mean ± SD, and P values were calculated using Student t test. *p < 0.05, ** p < 0.01, and *** p < 0.001

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