Fig. 3.

p53^R270H/MST1r axis confers drug tolerance to pancreatic cancer. (A‐C) RT‐qPCR (n = 2) and western blot display mRNA or protein level of MST1r following p53^R270H or p53^R172H silencing in KPC cells. Bars indicate SD. Experiments were repeated at least three times. A t‐test was calculated (P‐value < 0.05). (D) ChIP‐seq profile of histone post‐translational modifications, transcriptional factor (TF) binding and ATAC‐seq in the genomic region of mouse MST1r. (E‐G) ChIP‐qPCRs report p53^R270H binding (E), H2AZ content (F) or Brg1 binding (G) in the region corresponding to p63, ETS2 and Srepb1 (Sr.p1) binding (from panel (D) in KPC^R270H‐untreated cells (E) or following p53^R270H silencing (F and G). E and F report representative replicates of at least three independent biological replicates (bars indicate SD of technical replicates), G reports an average of fold over control of two independent biological replicates (bars indicate SE of biological replicates), two‐way ANOVA test was used, P‐values: * P < 0,05 and ** P < 0.01. (H,I) In vivo live‐cell imaging analysis by IncuCyte platform measured cell growth (phase contrast) and caspase‐3/7 activation (fluorescent green area) in KPC^R270H cells following MST1r silencing and gemcitabine (Gem) treatment. Scale bar indicates 200 microns. The data show a representative experiment of two biological replicates.