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Reprogramming pancreatic stellate cells via p53 activation: A putative target for pancreatic cancer therapy

Fig 3

p53 transcriptionally regulates the PSC activation network.

(A-B) Four primary human caPSCs were treated for 48h with Nutlin-3a or Nutlin-3b (control) and analyzed by RNA-seq. (A) Ingenuity Pathway Analysis (IPA) was performed on p53 downregulated and upregulated genes from RNA-seq analysis (fold change >1.5 or <0.67, adjusted p <0.05). The 5 most significant canonical pathways are shown and–log(pval) are indicated. (B) Heatmap representing selected genes from the RNA-seq analysis. Data are represented as log2 fold change, Nutlin-3a versus Nutlin-3b. (C-D) Primary mouse PSCs isolated from pancreata of wild-type C57B6/J mice were treated with Nutlin-3a or Nutlin-3b and harvested on day 3 (pre-activated) or on day 7 (activated) of culture. (C) Heatmap shows the relative abundance of selected genes from the RNA-seq analysis of Nutlin-3b treated mPSC (day 3 and 7) and Nutlin-3a treated mPSC (day 7). (D) IPA analysis was performed on p53 downregulated and upregulated genes at day 7 (fold change>1.5 or <0.67, adjpval<0.05). The 5 most significant canonical pathways are shown and -log(pval) are indicated.

Fig 3

doi: https://doi.org/10.1371/journal.pone.0189051.g003