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Embigin is overexpressed in pancreatic ductal adenocarcinoma and regulates cell motility through epithelial to mesenchymal transition via the TGF-β pathway.

 Dawoon E. Jung  ;  Jeong Mi Kim  ;  Chanyang Kim  ;  Si Young Song 
 MOLECULAR CARCINOGENESIS, Vol.55(5) : 633-645, 2016 
Journal Title
Issue Date
Animals ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology* ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; Membrane Glycoproteins/genetics* ; Membrane Glycoproteins/metabolism* ; Mice ; Molecular Chaperones/genetics* ; Molecular Chaperones/metabolism* ; Neoplasm Transplantation ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology* ; Signal Transduction ; Transforming Growth Factor beta/metabolism* ; Up-Regulation
Embigin ; Epithelial to Mesenchymal Transition ; Pancreatic ductal adenocarcinoma ; monocarboxylate transporter2 ; transforming growth factor-β
Embigin is a member of the immunoglobulin superfamily and encodes a transmembrane glycoprotein. There have been reports ofEmbigin involvement in neuromuscular junction formation and plasticity; however, the molecular functions of Embigin in other organs are unknown. Our aim was to investigate the possible role of Embigin in pancreatic cancer. In pancreatic ductal adenocarcinomatissues, Embigin expression was higher than that in normal pancreatic tissues. Immunohistochemical analysis revealed expression ofEmbigin in pancreatic cancer cells, as well as expression of monocarboxylate transporter 2 (MCT2) in cancer tissues. To gain further insight, we transfected BxPC-3 and HPAC pancreatic cancer cells with siRNA or shRNA targeting Embigin and observed reductions incell proliferation, migration, invasion, wound healing, and reduced levels of matrix metalloproteinases-2 and -9. Silencing of Embiginincreased intracellular L-lactate concentration by 1.5-fold and decreased MCT2 levels at the plasma membrane. Furthermore, Embiginsilencing led to a reduced expression of PI3K, GSK3-β, and Snail/Slug. Upon treating BxPC-3 cells with transforming growth factor-β (TGF-β), we observed elevated expression of Snail/Slug, Embigin, and Vimentin; meanwhile, when treating cells with SB-216763, a GSK3-β inhibitor, we noted decreases in GSK3-β, Snail/Slug, and Embigin expression, suggesting that the TGF-β signaling cascade, comprising PI3K, GSK3-β, Snail/Slug, and Embigin signals, mediates epithelial to mesenchymal transition (EMT) in pancreatic cancer cells. These findings indicate the involvement of Embigin in EMT in pancreatic cancer progression and suggest Embigin as a putative target for the detection and/or treatment of pancreatic cancer.
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5. Research Institutes (연구소) > Institute of Gastroenterology (소화기병연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Jeong Mi(김정미)
Song, Si Young(송시영) ORCID logo https://orcid.org/0000-0002-1417-4314
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