Skip to main content
. 2021 Jun;12(3):1180–1190. doi: 10.21037/jgo-21-283

Figure 4.

Figure 4

PADI1 affected the EMT process by regulating the ERK1/2-p38 signaling pathway in PAAD cells. The CFPAC-1 and HPAC cells were first treated with an ERK1/2 inhibitor (compound 27) and then transfected with siPADI1. (A) A wound-healing assay was performed to assess cell migration in the above two cell lines (40×). A Transwell assay was used to evaluate cell migration (B,C) and invasion (D,E) in the above two cell lines (100×, stained with crystal violet). Data are expressed as means ± SD from three independent experiments. ***, P<0.001, compared with the control. (F) The protein expression of E-cadherin, N-cadherin, Vimentin, p-ERK1/2, p38, and p-p38 was measured in the above two cell lines by a western-blot analysis. (G) PADI1 and p-ERK1/2 expression levels were observed using immunofluorescence (400×) in the above two cell lines. PADI1, peptidylarginine deiminase 1; EMT, epithelial-mesenchymal transition; PAAD, pancreatic ductal adenocarcinoma; SD, standard deviation.