Figure 1
From: TGFβ engages MEK/ERK to differentially regulate benign and malignant pancreas cell function
TGFβ receptors are necessary for ERK phosphorylation in the pancreas (a and b) Human pancreatic ductal adenocarcinoma (PDAC) and adjacent non-malignant samples were stained for pERK and scored by two investigators, showing increased ERK activity in 5/5 PDAC sections. The white arrow indicates cancer epithelium highly positive for pERK. (c and d) El-KRAS (KRAS) mice with mutant KRASG12D expression is restricted to the pancreas acinar compartment via a rat elastase promoter were employed as a model of early pancreatic tumorigenesis. These mice were crossed to mice conditionally expressing a dominant negative TGFBR2 in epithelial tissues (Tgfbr2DN) or heterozygous deletion of Tgfbr1 (Tgfbr1+/−) to form KT2 and KT1, respectively. Tissue sections were next stained for pERK, showing reduced expression in both KT2 and KT1 cohorts. (e–g) Tissues were next homogenized and analyzed by western blotting, confirming the observed pERK deficiency in KT2 and KT1 animals, as well as in Tgfbr2DN and Tgfbr1+/− mice with wild-type KRAS. (*P<0.05. n=4 mice per group unless otherwise specified).
