ArticleBrain pathology (Zurich, Switzerland)2011
Loss of the protein-tyrosine phosphatase DEP-1/PTPRJ drives meningioma cell motility.
Article in Brain pathology (Zurich, Switzerland), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.
- Meningioma animal models: a systematic review and meta-analysis.Journal of translational medicine · 2023Pooled it
- Integrated genomic analyses of acral and mucosal melanomas nominate novel driver genes.Genome medicine · 2022Pooled it
- RagC and Map4K3 deficiency in high-grade gliomas drives proliferation and modulates mTORC1-dependent cellular functions.Journal of neuropathology and experimental neurology · 2026Article
- Meis1 Targets Protein Tyrosine Phosphatase Receptor J in Fibroblast to Retard Chronic Kidney Disease Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Promoting the activity of a receptor tyrosine phosphatase with a novel pH-responsive transmembrane agonist inhibits cancer-associated phenotypes.Protein science : a publication of the Protein Society · 2023Article
- Review
- The effects of CD148 Q276P/R326Q polymorphisms in A431D epidermoid cancer cell proliferation and epidermal growth factor receptor signaling.Cancer reports (Hoboken, N.J.) · 2022Article
- Molecular neuropathology of brain-invasive meningiomas.Brain pathology (Zurich, Switzerland) · 2022Review
- Disrupting PTPRJ transmembrane-mediated oligomerization counteracts oncogenic receptor tyrosine kinase FLT3 ITD.Frontiers in oncology · 2022Article
- Review
- Association Between rs12037447, rs146732504, rs151078858, rs55723436, and rs6094136 Polymorphisms and Kawasaki Disease in the Population of Polish Children.Frontiers in pediatrics · 2021Article
- Article
- Molecular Mechanism and Approach in Progression of Meningioma.Frontiers in oncology · 2020Review
- Somatic inactivating PTPRJ mutations and dysregulated pathways identified in canine malignant melanoma by integrated comparative genomic analysis.PLoS genetics · 2018Article
- Thioredoxin reductase 1 and NADPH directly protect protein tyrosine phosphatase 1B from inactivation during HThe Journal of biological chemistry · 2017Article
- The intestinal barrier as an emerging target in the toxicological assessment of mycotoxins.Archives of toxicology · 2017Review
- The protein tyrosine phosphatase DEP-1/PTPRJ promotes breast cancer cell invasion and metastasis.Oncogene · 2015Article
- Review
- Deficiency of the protein-tyrosine phosphatase DEP-1/PTPRJ promotes matrix metalloproteinase-9 expression in meningioma cells.Journal of neuro-oncology · 2015Article
- In silico analyses reveal common cellular pathways affected by loss of heterozygosity (LOH) events in the lymphomagenesis of Non-Hodgkin's lymphoma (NHL).BMC genomics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.