Treatment with PS or AUY inhibits CXCR4-mediated signaling through AKT and ERK1/2 in cultured and primary AML cells. (A) OCI-AML3 cells were treated with the indicated concentrations of PS for 24 hours. After treatment, cells were lysed and immunoblot analyses were performed for CXCR4, GRK3, pAKT (Ser 473), AKT, pERK1/2, ERK1/2, and hsp70. The expression of β-actin in the lysates served as the loading control. (B) Primary AML cells were treated with the indicated concentrations of PS for 24 hours. After treatment, cell lysates were prepared and immunoblot analyses were performed for pAKT (Ser 473), AKT, pERK1/2, ERK1/2, and hsp70. The expression of β-actin in the lysates served as the loading control. (C) OCI-AML3 cells were treated with the indicated concentrations of AUY922 for 24 hours. After treatment, cells were lysed and immunoblot analyses were performed for CXCR4, AKT, and pERK1/2. The expression of β-actin in the lysates served as the loading control. (D) Primary AML cells were treated with the indicated concentrations of AUY922 for 24 hours. After treatment, cell lysates were prepared and immunoblot analyses were performed for CXCR4, GRK3, AKT, pERK1/2, ERK1/2, and hsp70. The expression of β-actin in the lysates served as the loading control.