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. 2014 Jun 13;9(6):e98867. doi: 10.1371/journal.pone.0098867

Figure 1. The p53 status interferes with the growth-inhibitory activity of ATO.

Figure 1

(A) Cells were left untreated or were irradiated with a single dose of 6 Gy. Four hours after IR, cells were harvested and their expression levels of p21 as a functional read-out for p53 transcriptional activity were determined by qRT-PCR. Relative quantification of p21 expression was done by normalization to the expression levels of porphobilinogen deaminase (PBGD) and to the untreated control using the ΔΔCt-method. IR-induced p21 expression (mean fold induction and standard error) is presented. The p53-deficient and p53-proficient cell lines were grouped using >1.5-fold induction of p21 by IR as threshold. (B, C) Cells were seeded at a density of 300 cells/well in 12-well plates and incubated for a period of 10–14 days in the absence or presence of the indicated doses of ATO. Survival fractions for given treatments were calculated on the basis of the survival of non-treated cells. Each sample was done in triplicate. The results from at least three independent experiments with p53-deficient (B) and p53-proficient cell lines (C) are presented. The symbols for each individual cell line are given in the graphs.