ArticleOncogenesis2016
GPR133 (ADGRD1), an adhesion G-protein-coupled receptor, is necessary for glioblastoma growth.
Article in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- mRNA markers for survival prediction in glioblastoma multiforme patients: a systematic review with bioinformatic analyses.BMC cancer · 2024Pooled it
- Subtype-Specific Prognostic and Molecular Significance of ADGRD1 in Lung Adenocarcinoma and Lung Squamous Cell Carcinoma.Current issues in molecular biology · 2026Article
- The therapeutic potential of orphan adhesion G-protein-coupled receptors.Nature reviews. Drug discovery · 2026Review
- Purinergic signaling promotes gliomagenesis through nuclear calcium transients.bioRxiv : the preprint server for biology · 2026Article
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Neuromechanobiology: Bridging Mechanobiology and Neuroscience Through Evidence and Open Questions.Cells · 2026Review
- ADGRD1 promotes bladder cancer progression and angiogenesis via the PI3K/AKT/mTOR-mediated pro-angiogenic secretome.Frontiers in oncology · 2026Article
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
- Circular RNA circNRIP1 promotes glioma progression by regulating the miR-106a-5p/GPR133 pathway.Scientific reports · 2025Article
- Von Hippel-Lindau/Hypoxia Inducible Factor Axis in Glioblastoma.International journal of molecular sciences · 2025Review
- Exogenous activation of the adhesion GPCR ADGRD1/GPR133 protects against bone loss by negatively regulating osteoclastogenesis.Science advances · 2025Article
- Modulation of GPR133 (ADGRD1) signaling by its intracellular interaction partner extended synaptotagmin 1.Cell reports · 2024Article
- Systematic characterization of multi-omics landscape between gut microbial metabolites and GPCRome in Alzheimer's disease.Cell reports · 2024Article
- Article
- The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability.Cell reports · 2023Article
- PTK7 is a positive allosteric modulator of GPR133 signaling in glioblastoma.Cell reports · 2023Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Activation of the adhesion G protein-coupled receptor GPR133 by antibodies targeting its N-terminus.The Journal of biological chemistry · 2022Article
- Article
- NFEBS open bio · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 3 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM) is a deadly primary brain malignancy with extensive intratumoral hypoxia. Hypoxic regions of GBM contain stem-like cells and are associated with tumor growth and angiogenesis. The molecular mechanisms that regulate tumor growth in hypoxic conditions are incompletely understood. Here, we use primary human tumor biospecimens and cultures to identify GPR133 (ADGRD1), an orphan member of the adhesion family of G-protein-coupled receptors, as a critical regulator of the response to hypoxia and tumor growth in GBM. GPR133 is selectively expressed in CD133+ GBM stem cells (GSCs) and within the hypoxic areas of PPN in human biospecimens. GPR133 mRNA is transcriptionally upregulated by hypoxia in hypoxia-inducible factor 1α (Hif1α)-dependent manner. Genetic inhibition of GPR133 with short hairpin RNA reduces the prevalence of CD133+ GSCs, tumor cell proliferation and tumorsphere formation in vitro. Forskolin rescues the GPR133 knockdown phenotype, suggesting that GPR133 signaling is mediated by cAMP. Implantation of GBM cells with short hairpin RNA-mediated knockdown of GPR133 in the mouse brain markedly reduces tumor xenograft formation and increases host survival. Analysis of the TCGA data shows that GPR133 expression levels are inversely correlated with patient survival. These findings indicate that GPR133 is an important mediator of the hypoxic response in GBM and has significant protumorigenic functions. We propose that GPR133 represents a novel molecular target in GBM and possibly other malignancies where hypoxia is fundamental to pathogenesis.
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.