Figure 1.
Bcr-Abl expression is associated with higher expression of hsp70 in human leukemia cells. (A) Western analyses of Bcr-Abl, hsp70, hsp90, Bcl-xL, Pim-2, Bag-1, and Bcl-2 in cell lines with expression of Bcr-Abl (K562, LAMA-84, Jurkat/Bcr-abl, HL-60/Bcr-Abl) and cell lines without expression of Bcr-Abl (HL-60/Neo, Jurkat). β-actin levels were used as the loading control. (B) Western analyses of Bcr-Abl, hsp70, and Bcl-xL in Jurkat/Bcr-Abl cells with doxycycline-inducible expression of Bcr-Abl. β-actin levels were used as the loading control. (C) Protein expression of Bcr-Abl, hsp70, and hsp90 in four samples of primary CML-BC leukemia cells. Cell lysates were immunoblotted with anti–Bcr-Abl, hsp70, and hsp90 antibodies. β-actin levels were used as loading control. (D) Western analysis of the heat shock factor-1 (HSF-1) and p-HSF-1 in cell lines with expression of Bcr-Abl (K562, LAMA-84, Jurkat/Bcr-abl, HL-60/Bcr-Abl) and without expression of Bcr-Abl (HL-60Neo, Jurkat/Neo). β-actin levels serve as the loading control. (E) RT-PCR analysis of mRNA expression of hsp70 in HL-60/Neo, HL-60/hsp70 (with ectopic overexpression of hsp70), Jurkat/Neo Jurkat/Bcr-abl, and HL-60/Bcr-Abl cells.β-actin mRNA served as the control. (F) Western analysis of p-HSF-1, HSF-1, and hsp70 performed on the cell lysates obtained from a representative sample of primary normal bone marrow progenitor cells (NBMPCs). β-actin levels were used as a loading control.