ArticleOncogene2015
The WIP1 oncogene promotes progression and invasion of aggressive medulloblastoma variants.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- REST elevation-dependent chromatin remodeling and alternative Grk6 transcript synthesis hyperactivates Cxcr4-Sdf1 signaling in cerebellar granule cell progenitors.bioRxiv : the preprint server for biology · 2025Article
- Identification of small molecule inhibitors of PPM1D using an integrated drug discovery platform.iScience · 2025Article
- Identification of Small Molecule Inhibitors of PPM1D Using a Novel Drug Discovery Platform.bioRxiv : the preprint server for biology · 2024Article
- Drivers Underlying Metastasis and Relapse in Medulloblastoma and Targeting Strategies.Cancers · 2024Review
- Clonal haematopoiesis - a novel entity that modifies pathological processes in elderly.Cell death discovery · 2023Review
- PPM1D in Solid and Hematologic Malignancies: Friend and Foe?Molecular cancer research : MCR · 2022Article
- Functionalized Macrophage Exosomes with Panobinostat and PPM1D-siRNA for Diffuse Intrinsic Pontine Gliomas Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Pathological implications of metabolic reprogramming and its therapeutic potential in medulloblastoma.Frontiers in cell and developmental biology · 2022Review
- Article
- Medulloblastoma: novel insights into emerging therapeutic targets.Expert opinion on therapeutic targets · 2021Article
- Potentiality of Protein phosphatase MgJournal of clinical laboratory analysis · 2020Article
- The molecular biology of medulloblastoma metastasis.Brain pathology (Zurich, Switzerland) · 2020Review
- Inhibition of mutant PPM1D enhances DNA damage response and growth suppressive effects of ionizing radiation in diffuse intrinsic pontine glioma.Neuro-oncology · 2019Article
- Integrative Proteomic and Phosphoproteomic Profiling of Testis from Wip1 Phosphatase-Knockout Mice: Insights into Mechanisms of Reduced Fertility.Molecular & cellular proteomics : MCP · 2019Article
- Role of wild-type p53-induced phosphatase 1 in cancer.Oncology letters · 2017Article
- Wip1-dependent modulation of macrophage migration and phagocytosis.Redox biology · 2017Article
- Wip1 is associated with tumorigenity and metastasis through MMP-2 in human intrahepatic cholangiocarcinoma.Oncotarget · 2017Article
- MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop.Oncotarget · 2017Article
- Clinical significance of Wip1 overexpression and its association with the p38MAPK/p53/p16 pathway in NSCLC.Molecular medicine reports · 2017Article
- LZAP is a novel Wip1 binding partner and positive regulator of its phosphatase activity in vitro.Cell cycle (Georgetown, Tex.) · 2017Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Recent studies suggest that medulloblastoma, the most common malignant brain tumor of childhood, is comprised of four disease variants. The WIP1 oncogene is overexpressed in Group 3 and 4 tumors, which contain medulloblastomas with the most aggressive clinical behavior. Our data demonstrate increased WIP1 expression in metastatic medulloblastomas, and inferior progression-free and overall survival of patients with WIP1 high-expressing medulloblastoma. Microarray analysis identified upregulation of genes involved in tumor metastasis, including the G protein-coupled receptor CXCR4, in medulloblastoma cells with high WIP1 expression. Stimulation with the CXCR4 ligand SDF1α activated PI-3 kinase signaling, and promoted growth and invasion of WIP1 high-expressing medulloblastoma cells in a p53-dependent manner. When xenografted into the cerebellum of immunodeficient mice, medulloblastoma cells with stable or endogenous high WIP1 expression exhibited strong expression of CXCR4 and activated AKT in primary and invasive tumor cells. WIP1 or CXCR4 knockdown inhibited medulloblastoma growth and invasion. WIP1 knockdown also improved the survival of mice xenografted with WIP1 high-expressing medulloblastoma cells. WIP1 knockdown inhibited cell surface localization of CXCR4 by suppressing expression of the G protein receptor kinase 5, GRK5. Restoration of wild-type GRK5 promoted Ser339 phosphorylation of CXCR4 and inhibited the growth of WIP1-stable medulloblastoma cells. Conversely, GRK5 knockdown inhibited Ser339 phosphorylation of CXCR4, increased cell surface localization of CXCR4 and promoted the growth of medulloblastoma cells with low WIP1 expression. These results demonstrate crosstalk among WIP1, CXCR4 and GRK5, which may be important for the aggressive phenotype of a subclass of medulloblastomas in children.
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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.