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. 2016 Sep 5;44(21):10259–10276. doi: 10.1093/nar/gkw791

Figure 5.

Figure 5.

Impact of ATM and DNA-PK inhibition on N-OH-PhIP triggered DDR and cytotoxicity. (A) Influence of ATM inhibition on N-OH-PhIP-induced DDR. Caco-2 cells were treated with N-OH-PhIP (10 μM) in the absence or presence of the ATM inhibitor (ATMi) KU-55933 for 14 h. Samples were then separated by SDS-PAGE followed by Western Blotting as indicated. Hsp90 served as loading control. (B) Effect of DNA-PK inhibition on N-OH-PhIP-induced DDR. Cells were treated with N-OH-PhIP (10 μM) with or without DNA-PK inhibitor (DNA-PKi) NU7026 for 14 h. Samples were then subjected to SDS-PAGE and western blot analysis was performed as indicated. Hsp90 was used as loading control. (C) Impact of ATM inhibition on cell viability. Caco-2 cells were incubated with 10 μM N-OH-PhIP with or without ATM inhibitor KU-55933 for 72 h and viability was determined (n = 5); ns: not significant. (D) Impact of DNA-PK inhibition on cell viability. Cells were incubated as described above with or without DNA-PK inhibitor (DNA-PKi) NU7026 for 72 h and viability was determined (n = 6); ns: not significant. (E) Impact of DNA-PKcs deficiency on cell viability. HCT116 cells proficient in DNA-PKcs (WT) and deficient in DNA-PKcs (DNA-PKcs−/−) were treated with or without 10 μM N-OH-PhIP and viability was measured after 72 h (n = 3); ns: not significant.