Linked Life Data

21691075

Source:http://linkedlifedata.com/resource/pubmed/id/21691075

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-6-21
pubmed:abstractText
KAI1/CD82, a tetraspanin membrane protein functions as a metastasis suppressor in many types of human cancers and has been shown to regulate cell adhesion properties. In the present study, we investigated the underlying mechanism of KAI1/CD82-mediated changes in cell adhesion to the extracellular matrix using human prostate cancer cells. We found that high KAI1/CD82 expression attenuated short-term cell adhesion to uncoated- or fibronectin-coated plates. Moreover, high KAI1/CD82 expression generated an extracellular environment unfavorable for cell adhesion as compared to low KAI1/CD82 expression, suggesting KAI1/CD82-dependent regulation of extracellular matrix (ECM) molecule(s) expression and/or secretion. Among ECM components examined, fibronectin exhibited decreased expression and secretion in high KAI1/CD82-expressing cells. Furthermore, high KAI1/CD82 expression interfered with the activation of ? (1) integrin at the cell surface while total ? (1) integrin levels remained unchanged, concomitant with reduced formation of focal adhesion complex and decreased bundling of actin filaments. Finally, high KAI1/CD82 expression significantly retarded cell motility in a scratch wound assay. Taken together, our results strongly suggest that KAI1/CD82 attenuates the activation of ? (1) integrin, and thereby down-regulates outside-in signaling of ? (1) integrin, leading to the reduction of focal adhesion formation and fibronectin expression/secretion, which subsequently interferes with cell adhesion properties and motility.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1421-9778
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 S. Karger AG, Basel.
pubmed:issnType
Electronic
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
575-86
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:21691075-Antigens, CD29, pubmed-meshheading:21691075-Antigens, CD82, pubmed-meshheading:21691075-Blotting, Western, pubmed-meshheading:21691075-Cell Adhesion, pubmed-meshheading:21691075-Cell Line, Tumor, pubmed-meshheading:21691075-Cell Movement, pubmed-meshheading:21691075-Extracellular Matrix, pubmed-meshheading:21691075-Fibronectins, pubmed-meshheading:21691075-Focal Adhesions, pubmed-meshheading:21691075-Gene Expression, pubmed-meshheading:21691075-Gene Silencing, pubmed-meshheading:21691075-Humans, pubmed-meshheading:21691075-Lipids, pubmed-meshheading:21691075-Male, pubmed-meshheading:21691075-Microscopy, Confocal, pubmed-meshheading:21691075-Plasmids, pubmed-meshheading:21691075-Prostatic Neoplasms, pubmed-meshheading:21691075-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:21691075-Signal Transduction, pubmed-meshheading:21691075-Transfection, pubmed-meshheading:21691075-Up-Regulation
pubmed:year
2011
pubmed:articleTitle
Metastasis suppressor KAI1/CD82 attenuates the matrix adhesion of human prostate cancer cells by suppressing fibronectin expression and ?1 integrin activation.
pubmed:affiliation
Medical & Bio-Material Research Center, College of Natural Sciences, School of Medicine, Kangwon National University, Chuncheon, Kangwon-do, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't