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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.

Authors
 Dawoon E. Jung  ;  Jeong Mi Kim  ;  Chanyang Kim  ;  Si Young Song 
Citation
 MOLECULAR CARCINOGENESIS, Vol.55(5) : 633-645, 2016 
Journal Title
MOLECULAR CARCINOGENESIS
ISSN
 0899-1987 
Issue Date
2016
MeSH
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
Keywords
Embigin ; Epithelial to Mesenchymal Transition ; Pancreatic ductal adenocarcinoma ; monocarboxylate transporter2 ; transforming growth factor-β
Abstract
Embiginis a member of the immunoglobulin superfamily and encodes a transmembrane glycoprotein. There have been reports ofEmbigininvolvement in neuromuscular junction formation and plasticity; however, the molecular functions ofEmbiginin other organs are unknown. Our aim was to investigate the possible role ofEmbigininpancreaticcancer. Inpancreaticductaladenocarcinomatissues,Embiginexpression was higher than that in normalpancreatictissues. Immunohistochemical analysis revealed expression ofEmbigininpancreaticcancer cells, as well as expression of monocarboxylate transporter 2 (MCT2) in cancer tissues. To gain further insight, we transfected BxPC-3 and HPACpancreaticcancer cells with siRNA or shRNA targetingEmbiginand observed reductions incellproliferation, migration, invasion, wound healing, and reduced levels of matrix metalloproteinases-2 and -9. Silencing ofEmbiginincreased 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, andEmbiginexpression, suggesting that the TGF-β signaling cascade, comprising PI3K, GSK3-β, Snail/Slug, andEmbiginsignals, mediatesepithelialtomesenchymaltransition(EMT) inpancreaticcancer cells. These findings indicate the involvement ofEmbiginin EMT inpancreaticcancer progression and suggestEmbiginas a putative target for the detection and/or treatment ofpancreaticcancer.
Full Text
http://onlinelibrary.wiley.com/doi/10.1002/mc.22309/abstract
DOI
10.1002/mc.22309
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 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
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146925
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