Infection with dominant negative (DN) STAT 5 sensitizes HL-60/hsp70 cells to Ara-C and etoposide-induced cell death. (A) HL-60/hsp70 cells were incubated with the media containing the vaccinia virus encoding DN-STAT5 cDNA for 4 hours (the mutant DN-STAT5 construct is phosphorylated and able to bind STAT5 DNA binding elements). Following this, cells were washed and exposed to Ara-C or etoposide for 24 hours. Subsequently, the control cells (infected with the control vaccinia virus or DN-STAT5 containing vaccinia virus) and the drug-treated cells were harvested to determine percent of dead cells (PI uptake by flow cytometry). Values represent the mean ± SE of 3 experiments. (B) Total cell lysates from the HL-60/hsp70 cells treated as above with the control virus or DN-STAT5 containing vaccinia virus followed by Ara-C were immunoblotted with antibodies specific for p-STAT5, Bcl-x_L, c-Myc, and hsp70. β-actin levels were used as loading control. (C) Molecular consequence of Bcr-Abl–mediated up-regulation of the levels and/or activity of AKT, STAT5, and hsp70 on the apoptotic signaling through the Apo-2L/TRAIL–induced DISC or the “apoptosome” downstream of the mitochondria.