Figure 3
Figure 3. Inhibition of PAK1 induces myelomonocytic differentiation of AML cells. (A) THP-1, MOLM-13, and HL-60 cells were treated with indicated concentrations of IPA-3 or FRAX-597 for 24 hours and analyzed by flow cytometry for expression of CD11b and CD15 cell surface markers for myelomonocytic differentiation. Y-axis plots fold change mean fluorescence intensity. Average of 2 independent experiments; error bars represent standard error of the mean. (B) Expression of CD11b and CD15 cell surface markers on THP-1 infected with lentiviruses targeting PAK1 for knockdown. (C) HL-60 AML cells were treated with indicated concentrations of DMSO (0.2%), IPA-3, or FRAX-597 for 24 hours. Cells were then spun onto slides (cytospin) and stained with Wright-Giemsa stain. (D) THP-1 AML cells were infected with lentivirus targeting PAK1 for knockdown or a nontargeting control and selected with puromycin. Cells were spun onto slides and stained with Wright-Giemsa stain.

Inhibition of PAK1 induces myelomonocytic differentiation of AML cells. (A) THP-1, MOLM-13, and HL-60 cells were treated with indicated concentrations of IPA-3 or FRAX-597 for 24 hours and analyzed by flow cytometry for expression of CD11b and CD15 cell surface markers for myelomonocytic differentiation. Y-axis plots fold change mean fluorescence intensity. Average of 2 independent experiments; error bars represent standard error of the mean. (B) Expression of CD11b and CD15 cell surface markers on THP-1 infected with lentiviruses targeting PAK1 for knockdown. (C) HL-60 AML cells were treated with indicated concentrations of DMSO (0.2%), IPA-3, or FRAX-597 for 24 hours. Cells were then spun onto slides (cytospin) and stained with Wright-Giemsa stain. (D) THP-1 AML cells were infected with lentivirus targeting PAK1 for knockdown or a nontargeting control and selected with puromycin. Cells were spun onto slides and stained with Wright-Giemsa stain.

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