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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Replication catastrophe is responsible for intrinsic PAR glycohydrolase inhibitor-sensitivity in patient-derived ovarian cancer models

Fig. 5

Drug sensitivity of OCMs. A Colony formation following 96 h of treatment with 1 μM PARGi or 1 μM PARPi or DMSO (Control). Representative images of 3 biological replicates. B Quantification of ca from (A) normalised to DMSO-treated cells (Control) and represented as fold-change. Mean of 3 biological replicates. C Proliferative Log EC50 values for PARGi and PARPi (Olaparib) in panel of seven OCMs. Means of 3 biological replicates. D Proliferative Log EC50 values for cisplatin and paclitaxel in panel of seven OCMs. Means of 3 biological replicates. E Proliferative Log EC50 values for PARGi, Olaparib (PARPi) and Niraparib for PARGi-sensitive OCMs (109 and 246). Mean of 3 biological replicates. F Dose-response curves for PARGi, Olaparib (PARPi) and Niraparib for PARGi-sensitive OCMs (109 and 246). Mean of 3 biological replicates. PRISM could not accurately calculate EC50 for PARGi-resistant cells, therefore for resistant OCMs the EC50 was approximated as 50 μM (half the maximal concentration tested). Error bars represent SEM. Statistics: 1-way ANOVA with Dunnett’s multiple comparisons test of PARGi versus Olaparib (P < 0.0001) and PARGi versus niraparib (P < 0.0001). * p < 0.05, ** p < 0.01, ****p < 0.0001. See also Supplementary Table 3, and Figs. S6 and S7

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