ArticleeLife2017
Negative regulation of urokinase receptor activity by a GPI-specific phospholipase C in breast cancer cells.
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- uPAR/suPAR Signaling and Organ Crosstalk in Cardiovascular-Kidney-Metabolic Syndrome.Circulation research · 2026Review
- Soluble urokinase plasminogen activator receptor promotes endoplasmic reticulum stress and apoptosis susceptibility through RAGE in sepsis acute kidney injury.Molecular medicine (Cambridge, Mass.) · 2025Article
- Metabolic traits shape responses to LSD1-directed therapy in glioblastoma tumor-initiating cells.Science advances · 2025Article
- A Contemporary Review of Plasminogen Activator Inhibitor Type 1: Structure, Function, Genetic Architecture, and Intracellular/Extracellular Roles.TH open : companion journal to thrombosis and haemostasis · 2025Review
- From Classical to Alternative Pathways of 2-Arachidonoylglycerol Synthesis: AlterAGs at the Crossroad of Endocannabinoid and Lysophospholipid Signaling.Molecules (Basel, Switzerland) · 2024Review
- Generation and Characterization of Novel Pan-Cancer Anti-uPAR Fluorescent Nanobodies as Tools for Image-Guided Surgery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Exploring the heterogeneity of osteosarcoma cell characteristics and metabolic states and their association with clinical prognosis.Frontiers in immunology · 2024Article
- Comprehensive analysis of the lncRNAs-related immune gene signatures and their correlation with immunotherapy in lung adenocarcinoma.British journal of cancer · 2023Article
- Elevated PLAUR is observed in the airway epithelium of asthma patients and blocking improves barrier integrity.Clinical and translational allergy · 2023Article
- An independent regulator of global release pathways in astrocytes generates a subtype of extracellular vesicles required for postsynaptic function.Science advances · 2023Article
- Nitric oxide hinders club cell proliferation through Gdpd2 during allergic airway inflammation.FEBS open bio · 2023Article
- (Patho)Physiology of Glycosylphosphatidylinositol-Anchored Proteins I: Localization at Plasma Membranes and Extracellular Compartments.Biomolecules · 2023Review
- Cell biology of protein-lipid conjugation.Cell structure and function · 2023Review
- Soluble urokinase-type plasminogen activator receptor in sickle cell disease-associated chronic kidney disease.Blood advances · 2023Article
- The Role of Reprogrammed Glucose Metabolism in Cancer.Metabolites · 2023Review
- Article
- suPAR: An Inflammatory Mediator for Kidneys.Kidney diseases (Basel, Switzerland) · 2022Review
- The distribution and function of GDE2, a regulator of spinal motor neuron survival, are disrupted in Amyotrophic Lateral Sclerosis.Acta neuropathologica communications · 2022Article
- Tiki proteins are glycosylphosphatidylinositol-anchored proteases.FEBS letters · 2022Article
- Update on Novel Targeted Therapy for Pleural Organization and Fibrosis.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The urokinase receptor (uPAR) is a glycosylphosphatidylinositol (GPI)-anchored protein that promotes tissue remodeling, tumor cell adhesion, migration and invasion. uPAR mediates degradation of the extracellular matrix through protease recruitment and enhances cell adhesion, migration and signaling through vitronectin binding and interactions with integrins. Full-length uPAR is released from the cell surface, but the mechanism and significance of uPAR shedding remain obscure. Here we identify transmembrane glycerophosphodiesterase GDE3 as a GPI-specific phospholipase C that cleaves and releases uPAR with consequent loss of function, whereas its homologue GDE2 fails to attack uPAR. GDE3 overexpression depletes uPAR from distinct basolateral membrane domains in breast cancer cells, resulting in a less transformed phenotype, it slows tumor growth in a xenograft model and correlates with prolonged survival in patients. Our results establish GDE3 as a negative regulator of the uPAR signaling network and, furthermore, highlight GPI-anchor hydrolysis as a cell-intrinsic mechanism to alter cell behavior.
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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.