Figure 5.
Figure 5. Cotreatment with LBH589 and 17-AAG induces more apoptosis of HL-60 cells with the wild-type p210Bcr-Abl or mutant p210T315I Bcr-Abl expressing leukemia cells. (A) HL-60/p210Bcr-Abl and HL-60/p210T315I cells were treated with the indicated concentrations of LBH589 and/or 17-AAG for 48 hours. Following this, the percentage of annexin-V-stained apoptotic cells was determined by flow cytometry. (B) Following treatment with 50 nM of LBH589 and/or 1000 nM 17-AAG for 24 hours, Western blot analyses of p21, Bcr-Abl, p-STAT5, STAT5, c-Raf-1, p-AKT, and AKT were performed in the cell lysates from wt p210Bcr-Abl or its mutant HL60/p210T315I expressing leukemia cells. The levels of β-actin served as the loading control.

Cotreatment with LBH589 and 17-AAG induces more apoptosis of HL-60 cells with the wild-type p210Bcr-Abl or mutant p210T315I Bcr-Abl expressing leukemia cells. (A) HL-60/p210Bcr-Abl and HL-60/p210T315I cells were treated with the indicated concentrations of LBH589 and/or 17-AAG for 48 hours. Following this, the percentage of annexin-V-stained apoptotic cells was determined by flow cytometry. (B) Following treatment with 50 nM of LBH589 and/or 1000 nM 17-AAG for 24 hours, Western blot analyses of p21, Bcr-Abl, p-STAT5, STAT5, c-Raf-1, p-AKT, and AKT were performed in the cell lysates from wt p210Bcr-Abl or its mutant HL60/p210T315I expressing leukemia cells. The levels of β-actin served as the loading control.

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