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. Author manuscript; available in PMC: 2017 Dec 12.
Published in final edited form as: Cancer Cell. 2016 Dec 12;30(6):940–952. doi: 10.1016/j.ccell.2016.11.006

Figure 6. Inhibition of β-lapachone-stimulated, NQO1-dependent PARP1 hyperactivation by Rucaparib spares catastrophic energy loss.

Figure 6

(A–D)NQO1+ A549 NSCLC cells were pretreated with Rucaparib (15 µM, 2 hr), then exposed or not to Rucaparib (15 µM) + β-lap (3 or 8 µM), ± dicoumarol (DIC, 50 µM) for 2 hr. Cells were also treated with β-lap (3 or 8 µM, 2 hr) alone. Cells were then monitored for: Long-term ROS formation (i.e., relative H2O2 levels) at 2 hr (A); Real-time oxygen consumption rates (OCRs) after various drug treatments (added at t=20 min, arrow) by Seahorse XF analyses: Ruc, Rucaparib; Oligo, oligomycin (B); Total NAD+ and NADH levels (C); and Relative ATP levels after 2 hr treatments (D). Results were separately repeated at least three times in triplicate each. Results (means ± SEM) from three independent experiments. ***, p < 0.001; **, p < 0.01; *, p < 0.05 (t tests).

See also Figures S5A–S5D.