Figure 4
From: TGFβ engages MEK/ERK to differentially regulate benign and malignant pancreas cell function
TGFβ engages pERK to direct both the cell cycle and EMT in benign pancreas duct cells. (a) HPDE cells were again starved of growth supplements and pre-incubated with U0126 prior to TGFβ-treatment. Cells were fixed after 72 h and evaluated by immunocytochemistry for SMAD4, indicating reduced nuclear accumulation in response to exogenous TGFβ1 when pERK was inhibited. (b) Cells were dual-stained for p21 and pERK, affirming the efficacy of U0126 and necessity of pERK for TGFβ1-induced upregulation of p21. (c) Cells were next evaluated for expression of proliferation surrogate PCNA as well as the p21 target CDK2, both of which were downregulated in response to TGFβ, but showed no change in response to both TGFβ and U0126. (d and e) HPDE cells were next assessed for changes in cell morphology via phase microscopy, and then stained for the epithelial marker E-Cadherin and the mesenchymal marker Vimentin, indicating that pERK is necessary for TGFβ-induced EMT.
