Fig. 2

Pancreas-specific Regnase-1 deletion promotes pancreatic oncogenesis with PMN-MDSC infiltration in mice. A-C Pancreatic phenotypes were examined in wild-type (WT) mice and pancreas-specific Kras- and Tp53-mutant (KPC) mice at 6 weeks of age. Representative images of HE staining (top) and CD11b immunostaining (bottom) in the pancreas of WT mice and pancreatic tumors of KPC mice (A). Number of CD11b-positive cells (B) (N = 6 per group) and relative Regnase-1 (Zc3h12a) mRNA levels (C) (N = 6 per group) in the pancreas of WT mice and pancreatic tumors of KPC mice. D-H Pancreatic phenotypes were examined in WT mice, pancreas-specific Regnase-1 knockout (PR) mice, pancreas-specific Kras-mutant (PK) mice, and pancreas-specific Kras-mutant Regnase-1 knockout (PKR) mice at 4 weeks of age. Macroscopic image (top) and HE staining (bottom) of the pancreas (D). Pancreatic weights in each group (E) (N = 6 per group). Kaplan–Meier curves of overall survival in each group (F) (N = 12 per group). Representative images of CD11b immunostaining (G left) and the number of CD11b-positive cells (G right) in each group (N = 6 per group). Relative mRNA levels (H) of Itgam, Ly6g, Arg1, Nos2, S100a8, and S100a9 in pancreatic tissue (N = 6 per group). One-way analysis of variance followed by Tukey's post hoc test was used to compare differences between the four groups. *: P < 0.05, Scale bars: 200 μm (insets)