Effects of XN4 on cell cycle arrest in CML cells.
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<p>(A) Representation of apoptosis ratio after XN4 treatment for 12 h. (B) Effects of XN4 on the activation of DNA-damage-sensing kinases in CML cells. K562 and K562/G01 cells were treated with 6 μM XN4 for 12 h, with or without NAC pre-treatment. The data demonstrate that XN4 increased the phosphorylation level of rH2AX and ATM, but decreased CDK2 and CyclinE1; β-Actin served as the protein-loading control. 1. control; 2. XN4 6 μM; 3. NAC 5 mM; 4. NAC 5 mM+XN4 6 μM. (C-E) K562 and K562/G01 cells were cultured in the presence of XN4 for 48 h, with or without pre-treatment with 5 mM NAC for 1 h, harvested, and then stained with PI and subsequently analyzed by flow cytometry with quantitation using the FlowJo software. (F) Representation of the fluorescence shift of BrdU after XN4 treatment, with or without NAC pre-treatment. K562 and K562/G01 cells were treated with 6 μM XN4 for 12 h, 5 mM NAC for 12 h, or 5 mM NAC for 1 h followed by 6 μM XN4 for 12 h. After the treatment, the cells were labeled with BrdU for 30 min, washed, and then incubated with 5μl of an PerCP-Cy5.5-conjugated anti-BrdU antibody for 20 minutes at room temperature. The cells were washed once more before flow cytometry (G) Quantification of the fluorescence shift of BrdU The data are expressed as the mean±SD. (** <i>p<</i>0.01, * <i>p<</i>0.05 vs control group, <i>p</i> = NS no significance, n = 3).</p