FIG. 3.

Overexpression of RAD51 only partially restored therapeutic drug resistance of BCR/ABL cells treated with STI571. 32Dcl3 cells (Parental) and BCR/ABL-expressing cells were infected with a retrovirus encoding RAD51-IRES-GFP (Parental+RAD51 and BCR/ABL+RAD51 cells, respectively) or IRES-GFP (Parental and BCR/ABL cells, respectively). GFP-positive cells were isolated by fluorescence-activated cell sorting, and the ABL kinase-selective inhibitor STI571 (1 μM) was added (+) or not (−) for 24 h in the presence of IL-3. (A) Expression of RAD51 and tyrosine phosphorylation of cellular proteins were examined by immunoblotting with anti-RAD51 antibody and antiphosphotyrosine antibody, respectively. Results are representative of two independent experiments. (B) Cells were plated in methylcellulose in the presence of IL-3 with the indicated concentrations of cisplatin or mitomycin C. Colonies were counted 7 days later. Results show the percentage of clonogenic cells (mean ± SD) from three independent experiments.