Skip to main content
. 2016 Nov 26;7(52):87417–87430. doi: 10.18632/oncotarget.13654

Figure 4. BMN673 and Olaparib induce preferential increases in γ-H2AX and cleaved Caspase-3 signal intensities in RAD54B-deficient cells.

Figure 4

A. Representative low resolution images depicting the abundance of γ-H2AX in cells treated with DMSO, IR, BMN673 or Olaparib. All images were acquired 48 h post treatments using the identical exposure times and thus changes in fluorescence intensities reflect changes in the global abundance of γ-H2AX (i.e. DNA DSBs). Nuclei and γ-H2AX are pseudocolored red and green, respectively, within the merge. Scale bar represents 10 μm. B. Scatter plots presenting the total γ-H2AX signal intensities from individual RAD54B-proficient (black circles) and RAD54B-deficient (grey circles) cells treated with DMSO (negative control), IR (positive control), BMN673 or Olaparib as determined by semi-quantitative IIF microscopy. A minimum of 175 cells were imaged per condition and the red bars identify the mean γ-H2AX signal intensity. Student's t-tests reveal statistically significant increases in γ-H2AX signal intensities in the RAD54B-deficient cells treated with BMN673 and Olaparib relative to corresponding RAD54B-proficient controls. (ns, not significant; **, P-value <0.01; ****, P-value <0.0001). Experiments were repeated two additional times. C. Bar graph presenting the mean (±SD) percentage of RAD54B-proficient (black) and RAD54B-deficient (grey) cells labeled with cleaved Caspase-3 following treatment with DMSO, Staurosporine (positive control), BMN673 or Olaparib. Student's t-tests reveal statistically significant increases in the percentage of RAD54B-deficient cells labeled with cleaved Caspase-3 following BMN673 and Olaparib treatments relative to corresponding RAD54B-proficient controls. (ns, not significant; *, P-value <0.05). Experiments were repeated two additional times.