PADI1 contributes to epithelial-mesenchymal transition in pancreatic ductal adenocarcinoma through activating ERK1/2-p38 signaling pathway

Abstract Background Peptidylarginine deiminase 1 (PADI1) may be relative with the progression of epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma (PAAD). We aim to explore the role of PADI1 in PAAD. Methods The expression pattern of PADI1 in PAAD tissues and normal tissues was analyzed using The Cancer Genome Atlas (TCGA) dataset. PADI1 was knocked down in CFPAN-1 and HPAC cells, while overexpressed in PANC-1 and Bxpc-3 cells by RNA interference. Wound healing assay was performed to analyze relative cell migration distance. Cell migration and invasion were assessed by Transwell assay. Related protein expression levels were measured by western blot and immunofluorescence. Results Bioinformatics analysis showed that PADI1 was overexpressed in PAAD tissues and associated with worse survival prognosis. Knockdown of PADI1 suppressed the cell migration, invasion and activated ERK1/2-p38 signaling pathway in CFPAN-1 and HPAC cells. Overexpression of PADI1 obtained the opposite results in PANC-1 and Bxpc-3 cells. Moreover, treatment with MEK1/2 inhibitor significantly recovered the effects of PADI1 knockdown on cell migration, invasion, EMT process and p-ERK1/2 and p38 expression in CFPAN-1 and HPAC cells. Conclusions Our data suggested that PADI1 may function as an oncogene in regulating metastasis in vitro in PAAD.