dCK deficiency in resistant HL60R cells. (A) DAC hypomethylation induction in HL60D and DAC-resistant HL60R. We treated the cells with DAC (0.2-50 μM) and measured LINE methylation by bisulfite pyrosequencing analysis. (B) RILgene expression. (C) Inhibition of AZA of cell growth. Cells were treated with AZA (0.25-25 μM), and cell viability was measured by trypan blue exclusion. (D) LINE hypomethylation after AZA treatment. (E) Ara-CTP production, as measured by HPLC analysis using [³H] Ara-C as a substrate, was lost in HL60R-resistant cells. (F) dCK activity, as measured by phosphorylation of [³H]Ara-C in cell extracts, was also lost in resistant cells. (G) dCK protein expression was measured by Western blot analysis. β-Actin served as a control. (H) DCK mRNA expression was measured by quantitative PCR.