Figure 2
Figure 2. The CRM1 inhibitor KPT-185 inhibits the growth of AML cell lines through cell cycle arrest and apoptosis induction. (A) AML cell lines with wild-type p53 (OCI-AML-3, MOLM-13, and MV4;11) or mutant p53 (NB4, HL-60, KG-1, THP-1, and U937) cells were incubated with 100, 200, or 500 nM for 72 hours, and the annexin V–positive fractions were measured by flow cytometry (black bars). Cells were treated in parallel with 5 µM Nutlin-3a (white bars). Results are expressed as mean ± SD. (B) Lentivirally transduced wild-type p53 AML cells (virus encoding either control shRNA [shC] or p53-specific shRNA [shp53]) were incubated with 0, 10, 20, 50, 100, 200, 500, or 1000 nM of KPT-185 for 72 hours, and the numbers of viable cells and annexin V–positive fractions were measured. *P < .05; **P < .01; ***P < .001.

The CRM1 inhibitor KPT-185 inhibits the growth of AML cell lines through cell cycle arrest and apoptosis induction. (A) AML cell lines with wild-type p53 (OCI-AML-3, MOLM-13, and MV4;11) or mutant p53 (NB4, HL-60, KG-1, THP-1, and U937) cells were incubated with 100, 200, or 500 nM for 72 hours, and the annexin V–positive fractions were measured by flow cytometry (black bars). Cells were treated in parallel with 5 µM Nutlin-3a (white bars). Results are expressed as mean ± SD. (B) Lentivirally transduced wild-type p53 AML cells (virus encoding either control shRNA [shC] or p53-specific shRNA [shp53]) were incubated with 0, 10, 20, 50, 100, 200, 500, or 1000 nM of KPT-185 for 72 hours, and the numbers of viable cells and annexin V–positive fractions were measured. *P < .05; **P < .01; ***P < .001.

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