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. Author manuscript; available in PMC: 2015 Aug 13.
Published in final edited form as: Cancer Res. 2013 Nov 18;74(4):1153–1165. doi: 10.1158/0008-5472.CAN-13-0955

Figure 1. Prodigiosin and compound R induce p53-like transcriptional activity in p53-mutant and p53-null human cancer cells.

Figure 1

(A), The structures of prodigiosin (P) and compound R (R). (B), SW480, DLD1 and HCT116 p53−/− cells with p53-responsive reporter were treated with different concentrations of “P”, “R” or DMSO control for 2, 20 and 72 hr. p53-responsive reporter activity was imaged by the IVIS imaging system after treatment. (red/green/blue color indicates bioluminescent signal from p53 responsive luciferase reporter, lack of signal (black) indicates absence of cells due to cell death). (C), Prodigiosin and compound R induce endogenous p53 target genes DR5, PUMA and p21. SW480 and HCT116 p53−/− cells were treated with the indicated concentrations of “P” or “R” for 12 hr. DR5, PUMA and p21 were detected by Western Blotting. Ran protein expression was used as the loading control.