Figure 3.

Activation of p53 and cell death induced by the DNA topoisomerase I inhibitors camptothecin and β-lapachone. (A) A type I SMA fibroblasts as described [29] were treated with 25 μM camptothecin and levels of p53 were analyzed by Western blotting. The same blots were stripped and reprobed with anti-β-tubulin antibodies as a loading control. (B) A type II/III SMA fibroblasts as described [29] were treated with 10 μM menadione and levels of p53 were analyzed as described for (A). (C) Control and SMA fibroblasts were treated with 25 μM camptothecin or 25 μM β-lapachone and levels of p53 were analyzed as described for (A). Relative ratios of p53 to tubulin levels are indicated. (D) Three control and three SMA fibroblasts (one type I, one type II, and one type III) were treated with camptothecin for 72 h or β-lapachone for 24 h at the indicated concentrations, respectively. Cell survival of treated cells was measured by the CellTiter-Blue assay, and the relative cell viability was calculated and presented as percentage of the untreated cells. Each condition was set up as replicates of four and repeated three times. The data presented here are combined mean values ± sem for three control and three SMA fibroblasts. Statistical analyses (unpaired t test) indicate that SMA fibroblasts are significantly sensitive to camptothecin at each tested concentration than control fibroblasts (*** p < 0.0001 and ** p < 0.001). CPT = camptothecin, β-LP = β-lapachone, MENA = menadione, and ND = non-detected.

Wu et al. BMC Cell Biology 2009 10:40   doi:10.1186/1471-2121-10-40
Download authors' original image