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. 2012 Aug 20;3(8):851–865. doi: 10.18632/oncotarget.586

Figure 7. Effect of modulation of NBS1, nucleosides or H2AX during inhibition of HH signaling at the level of GLI.

Figure 7

A. In transient transfections, HT29 cells were transfected with the retroviral vector pQCXIH alone, or pQCXIH-NBS1 for 24 hr prior to treatment for 48 hr with GANT61 at concentrations of 0 μM, 5 μM, 10 μM, or 20 μM. Cell death was determined. Inset: Total NBS1 and p-NBS1Ser343 expression was analyzed by western analysis. B: HT29 cells were treated with 20 μM concentrations of each of adenosine, guanosine, cytidine and thymidine simultaneously with GANT61 (20 μM) for 72 hr, and the extent of cell death determined. C: HT29 cells stably expressing H2AXshRNA or scrambled shRNA were treated with increasing concentrations of GANT61 for 48 hr at which time the extent of cell death was determined. Inset: H2AX knockdown was confirmed by western analysis. D. HT29 cells stably expressing scrambled shRNA or H2AXshRNA were treated with GANT61 (20 μM) for up to 24 hr, and the expression of γH2AX determined by western analysis. β-actin was used as the loading control.