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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Gynecol Oncol. 2019 Jan 25;153(1):127–134. doi: 10.1016/j.ygyno.2019.01.015

Figure 1. 53BP1 loss and PARP inhibitor sensitivity in HR-deficient ovarian cancer cells.

Figure 1.

A, expression of 53BP1 of was assessed by immunoblotting in whole cell lysates of COV362 transduced with empty vector (EV) or sgRNA targeting 53BP1−/− as well as OV90 and PE01 cells. B, homologous recombination repair was assayed using the DR-GFP plasmid as described in the Methods and illustrated in Fig. S1. OV90 (HR proficient—ref. 24) and PE01 cells (HR deficient–refs. 11 and 23) served as controls for this assay. Error bars, summary of 4 independent assays. PARPi sensitivity of the positive and negative controls is shown in Fig. S1C. C, COV362 empty vector (EV) and COV362 53BP1−/− cells were continuously exposed to increasing concentrations of PARP inhibitor veliparib in a clonogenic assay. Error bars, ± SEM from triplicate plates in a single assay. Across 5 independent assays, the IC50 for veliparib was 2.9 ± 0.4-fold (mean ± SEM) higher in the 53BP1−/− cells.