Cited 16 times in
Embigin is overexpressed in pancreatic ductal adenocarcinoma and regulates cell motility through epithelial to mesenchymal transition via the TGF-β pathway.
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김정미 | - |
dc.contributor.author | 송시영 | - |
dc.contributor.author | 정다운 | - |
dc.date.accessioned | 2017-02-27T07:35:09Z | - |
dc.date.available | 2017-02-27T07:35:09Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 0899-1987 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/146925 | - |
dc.description.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. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.format.extent | 633~645 | - |
dc.language | English | - |
dc.publisher | Wiley-Liss | - |
dc.relation.isPartOf | MOLECULAR CARCINOGENESIS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Carcinoma, Pancreatic Ductal/genetics | - |
dc.subject.MESH | Carcinoma, Pancreatic Ductal/metabolism | - |
dc.subject.MESH | Carcinoma, Pancreatic Ductal/pathology* | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Cell Movement | - |
dc.subject.MESH | Cell Proliferation | - |
dc.subject.MESH | Epithelial-Mesenchymal Transition | - |
dc.subject.MESH | Gene Expression Regulation, Neoplastic | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Membrane Glycoproteins/genetics* | - |
dc.subject.MESH | Membrane Glycoproteins/metabolism* | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Molecular Chaperones/genetics* | - |
dc.subject.MESH | Molecular Chaperones/metabolism* | - |
dc.subject.MESH | Neoplasm Transplantation | - |
dc.subject.MESH | Pancreatic Neoplasms/genetics | - |
dc.subject.MESH | Pancreatic Neoplasms/metabolism | - |
dc.subject.MESH | Pancreatic Neoplasms/pathology* | - |
dc.subject.MESH | Signal Transduction | - |
dc.subject.MESH | Transforming Growth Factor beta/metabolism* | - |
dc.subject.MESH | Up-Regulation | - |
dc.title | Embigin is overexpressed in pancreatic ductal adenocarcinoma and regulates cell motility through epithelial to mesenchymal transition via the TGF-β pathway. | - |
dc.type | Article | - |
dc.publisher.location | United States | - |
dc.contributor.college | Researcher Institutes | - |
dc.contributor.department | Institute of Gastroenterology | - |
dc.contributor.googleauthor | Dawoon E. Jung | - |
dc.contributor.googleauthor | Jeong Mi Kim | - |
dc.contributor.googleauthor | Chanyang Kim | - |
dc.contributor.googleauthor | Si Young Song | - |
dc.identifier.doi | 10.1002/mc.22309 | - |
dc.contributor.localId | A00882 | - |
dc.contributor.localId | A02035 | - |
dc.relation.journalcode | J02255 | - |
dc.identifier.eissn | 1098-2744 | - |
dc.identifier.pmid | 25773908 | - |
dc.identifier.url | http://onlinelibrary.wiley.com/doi/10.1002/mc.22309/abstract | - |
dc.subject.keyword | Embigin | - |
dc.subject.keyword | Epithelial to Mesenchymal Transition | - |
dc.subject.keyword | Pancreatic ductal adenocarcinoma | - |
dc.subject.keyword | monocarboxylate transporter2 | - |
dc.subject.keyword | transforming growth factor-β | - |
dc.contributor.alternativeName | Kim, Jeong Mi | - |
dc.contributor.alternativeName | Song, Si Young | - |
dc.contributor.alternativeName | Jung, Dawoon E. | - |
dc.contributor.affiliatedAuthor | Kim, Jeong Mi | - |
dc.contributor.affiliatedAuthor | Song, Si Young | - |
dc.citation.volume | 55 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 633 | - |
dc.citation.endPage | 645 | - |
dc.identifier.bibliographicCitation | MOLECULAR CARCINOGENESIS, Vol.55(5) : 633-645, 2016 | - |
dc.date.modified | 2017-02-24 | - |
dc.identifier.rimsid | 46490 | - |
dc.type.rims | ART | - |
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