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  • Loss of the protein-tyrosine phosphatase DEP-1/PTPRJ drives meningioma cell motility.

Loss of the protein-tyrosine phosphatase DEP-1/PTPRJ drives meningioma cell motility.

Brain pathology (Zurich, Switzerland) (2010-11-26)
Astrid Petermann, Daniela Haase, Andrea Wetzel, Kamal K Balavenkatraman, Tencho Tenev, Karl-Heinz Gührs, Sabrina Friedrich, Makoto Nakamura, Christian Mawrin, Frank-D Böhmer
ABSTRACT

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.

MATERIALS
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Product Description

Sigma-Aldrich
Anti-PTPRJ antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution