Figure 2.

DSB repair stimulation by chemotherapeutics as a function of NF-κB activity. (A) K562(Δ/3′) cells were co-transfected with pCMV-I-SceI and pcDNA3.0-IκBα-SR/pcDNA3.0 as indicated, cultivated for 24 h and then treated with 50 μM etoposide (Eto). Cells were further cultivated for 48 h, when HR assays were performed. DSB repair frequencies in DMSO-treated controls were defined as 100% (absolute mean value 2 × 10⁻³). Mean values and SEMs from n = 9 (*P < 0.05; **P < 0.01). (B and C) The percentages of cells with sub-G1 DNA content (B) in G1, S or G2 cell cycle phases (C) were determined with propidium iodide-stained cells at the time point of the repair measurements. Columns, mean values of n = 4; bars SEMs. (D) IκBα phosphorylation in cells exposed to 50 μM etoposide was analysed by western blotting (p- IκBα). (E–H) K562(Δ/3′) cells were co-transfected with pCMV-I-SceI and pcDNA3.0-IκBα-SR/pcDNA3.0, treated with 300 nM camptothecin (Cpt) and evaluated as in (A–D). Note that IκBα degradation interfered with p-IκBα detection 24 h after camptothecin addition in (H).