Linked Life Data

20878057

Source:http://linkedlifedata.com/resource/pubmed/id/20878057

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-9-29
pubmed:abstractText
The Wnt/?-catenin pathway plays a critical role in cell proliferation and oncogenesis. To clarify the role of cytoplasmic accumulation of ?-catenin in oral squamous cell carcinoma (SCC), the cDNA of a mutant form of ?-catenin that lacks the entire region with the glycogen synthase kinase-3 ? (GSK-3?)-specific phosphorylation site was transfected into Ca9-22 cells whose ?-catenin had been expressed predominantly at the membrane, and permanent cell lines expressing aberrant ?-catenin in the cytoplasm and nucleus were produced. These transfectants, C1 and C5, proliferated at similar rates to the parental Ca9-22 cells, but the cell morphology changed from polygonal to spindle-shaped and close cell-cell interaction was lost. These mutant ?-catenin-expressing cells exhibited a significantly higher invasion/migration capacity than wild-type Ca9-22 cells. The transcriptional activities of this mutant ?-catenin form was enhanced in these cells which could be demonstrated by an elevated level of the transcription factor T-cell factor (Tcf)/lymphoid enhancer factor (Lef)-dependent reporter gene activity as well as by the up-regulation of Wnt/?-catenin target gene matrix metalloproteinase (MMP)-7. Moreover, we observed the redistribution of E-cadherin, the rearrangement of actin filaments, and the elevation of active Rho family members, Cdc42 and Rac. These results suggest that aberrant cytoplasmic accumulation of ?-catenin can induce Tcf/Lef-mediated transcriptional activity, up-regulate MMP-7, and induce epithelial and mesenchymal transition (EMT). This would enhance the invasion and migration of oral SCC cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1791-2423
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1095-103
pubmed:meshHeading
pubmed-meshheading:20878057-Blotting, Western, pubmed-meshheading:20878057-Carcinoma, Squamous Cell, pubmed-meshheading:20878057-Cell Line, Tumor, pubmed-meshheading:20878057-Cell Movement, pubmed-meshheading:20878057-Epithelial-Mesenchymal Transition, pubmed-meshheading:20878057-Gene Expression Regulation, Neoplastic, pubmed-meshheading:20878057-Humans, pubmed-meshheading:20878057-Lymphoid Enhancer-Binding Factor 1, pubmed-meshheading:20878057-Matrix Metalloproteinase 7, pubmed-meshheading:20878057-Mouth Neoplasms, pubmed-meshheading:20878057-Neoplasm Invasiveness, pubmed-meshheading:20878057-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20878057-Signal Transduction, pubmed-meshheading:20878057-Transfection, pubmed-meshheading:20878057-Wnt Proteins, pubmed-meshheading:20878057-beta Catenin
pubmed:year
2010
pubmed:articleTitle
Involvement of the Wnt-?-catenin pathway in invasion and migration of oral squamous carcinoma cells.
pubmed:affiliation
Department of Oral and Maxillofacial Surgery II, Osaka University Graduated School of Dentistry, Suita, Osaka 565-0871, Japan. s-iwai@dent.osaka-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't