Source:http://linkedlifedata.com/resource/pubmed/id/21091576
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2011-6-14
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| pubmed:abstractText |
DEP-1/PTPRJ is a transmembrane protein-tyrosine phosphatase which has been proposed as a suppressor of epithelial tumors. We have found loss of heterozygosity (LOH) of the PTPRJ gene and loss of DEP-1 protein expression in a subset of human meningiomas. RNAi-mediated suppression of DEP-1 in DEP-1 positive meningioma cell lines caused enhanced motility and colony formation in semi-solid media. Cells devoid of DEP-1 exhibited enhanced signaling of endogenous platelet-derived growth factor (PDGF) receptors, and reduced paxillin phosphorylation upon seeding. Moreover, DEP-1 loss caused diminished adhesion to different matrices, and impaired cell spreading. DEP-1-deficient meningioma cells exhibited invasive growth in an orthotopic xenotransplantation model in nude mice, indicating that elevated motility translates into a biological phenotype in vivo. We propose that negative regulation of PDGF receptor signaling and positive regulation of adhesion signaling by DEP-1 cooperate in inhibition of meningioma cell motility, and possibly tumor invasiveness. These phenotypes of DEP-1 loss reveal functions of DEP-1 in adherent cells, and may be more generally relevant for tumorigenesis.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
|
| pubmed:issn |
1750-3639
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| pubmed:author |
pubmed-author:BöhmerFrank-DFD,
pubmed-author:BalavenkatramanKamal KKK,
pubmed-author:FriedrichSabrinaS,
pubmed-author:GührsKarl-HeinzKH,
pubmed-author:HaaseDanielaD,
pubmed-author:MawrinChristianC,
pubmed-author:NakamuraMakotoM,
pubmed-author:PetermannAstridA,
pubmed-author:TenevTenchoT,
pubmed-author:WetzelAndreaA
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| pubmed:copyrightInfo |
© 2010 The Authors. Brain Pathology © 2010 International Society of Neuropathology.
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| pubmed:issnType |
Electronic
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| pubmed:volume |
21
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
405-18
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| pubmed:meshHeading |
pubmed-meshheading:21091576-Animals,
pubmed-meshheading:21091576-Cell Adhesion,
pubmed-meshheading:21091576-Cell Line, Tumor,
pubmed-meshheading:21091576-Cell Movement,
pubmed-meshheading:21091576-Gene Knockdown Techniques,
pubmed-meshheading:21091576-Humans,
pubmed-meshheading:21091576-Immunoblotting,
pubmed-meshheading:21091576-Immunohistochemistry,
pubmed-meshheading:21091576-Loss of Heterozygosity,
pubmed-meshheading:21091576-Meningeal Neoplasms,
pubmed-meshheading:21091576-Meningioma,
pubmed-meshheading:21091576-Mice,
pubmed-meshheading:21091576-Mice, Nude,
pubmed-meshheading:21091576-Neoplasm Invasiveness,
pubmed-meshheading:21091576-Paxillin,
pubmed-meshheading:21091576-Polymerase Chain Reaction,
pubmed-meshheading:21091576-RNA, Small Interfering,
pubmed-meshheading:21091576-Receptor-Like Protein Tyrosine Phosphatases, Class 3,
pubmed-meshheading:21091576-Signal Transduction,
pubmed-meshheading:21091576-Transfection
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| pubmed:year |
2011
|
| pubmed:articleTitle |
Loss of the protein-tyrosine phosphatase DEP-1/PTPRJ drives meningioma cell motility.
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| pubmed:affiliation |
Institute of Molecular Cell Biology, Center for Molecular Biomedicine, Jena, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|