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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: p53-Dependent PUMA to DRAM antagonistic interplay as a key molecular switch in cell-fate decision in normal/high glucose conditions

Fig. 1

High glucose (HG) switched the adriamycin (ADR)-induced p53 transcriptional activity from PUMA to DRAM. (a) RKO and HCT116 cells were kept in low glucose (LG) or high glucose (HG) medium for 24 h and then treated with ADR (2 μg/ml) for 16 h before being assayed for semi-quantitative RT-PCR analysis of PUMA and DRAM gene expression. 28S was used as a control for efficiency of RNA extraction and transcription. Histograms representing quantification of PUMA or DRAM/28S ratio as assessed by densitometric analysis are shown. Densitometric values were quantified using the ImageJ software and normalized to control. The values of control were set to 1. The data are presented as means ± S.D. of three independent experiments. *P < 0.001. (b) RKO and HCT116 cells were treated with ADR (2 μg/ml) for 16 h in LG and HG medium, with or without p53 inhibitor pifithrin-α (PFT-α) (30 μM) before being assayed for semi-quantitative RT-PCR analysis of PUMA and DRAM gene expression. 28S was used as a control for efficiency of RNA extraction and transcription. One representative experiment is shown. (c) HCT116-p53−/− cells were treated and assayed as in (a)

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