Fig. 1: Rucaparib exerts differential cytotoxicity, induces replication stress (RS) and activates ATR, CHK1 and WEE1 in the cell panel. | British Journal of Cancer

Fig. 1: Rucaparib exerts differential cytotoxicity, induces replication stress (RS) and activates ATR, CHK1 and WEE1 in the cell panel.

From: ATR, CHK1 and WEE1 inhibitors cause homologous recombination repair deficiency to induce synthetic lethality with PARP inhibitors

Fig. 1

a Colony formation-based cell survival following exposure of cells to the indicated concentration of rucaparib for 24 h. Data, percent survival relative to vehicle (DMSO) control, are mean ± SEM of 3 independent experiments. b Induction of RS following exposure of cells to 10 µM rucaparib for 24 h, measured by γH2AX foci/cell. Representative images of paired cell lines are shown. c Mean data from 3 independent experiments of the type shown in Fig. 1b, significant induction by rucaparib is shown by †p < 0.05, ††p < 0.01, †††p < 0.0001 (scatter plots in supplementary 1 C). d Induction of phosphorylation of CHK1 S345, CHK1 S296 and CDK1 Y15 following exposure to 10 µM rucaparib for 24 h determined by Western blotting. Representative blots are shown. e–g Pooled data for all cell lines from 3 independent experiments of the type shown in 1D. Each bar represents mean and standard error of expression normalised to vinculin loading control.

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