ArticleMolecular cancer research : MCR2012
Suppression of G-protein-coupled receptor kinase 3 expression is a feature of classical GBM that is required for maximal growth.
Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- TRIM58 downregulation maintains stemness via MYH9-GRK3-YAP axis activation in triple-negative breast cancer stem cells.Cancer gene therapy · 2024Article
- GRK3 is a poor prognosticator and serves as a therapeutic target in advanced gastric adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2022Article
- NPY1R exerts inhibitory action on estradiol-stimulated growth and predicts endocrine sensitivity and better survival in ER-positive breast cancer.Scientific reports · 2022Article
- The GRKs Reactome: Role in Cell Biology and Pathology.International journal of molecular sciences · 2021Review
- Article
- G protein-coupled receptor kinase 5 modifies cancer cell resistance to paclitaxel.Molecular and cellular biochemistry · 2019Article
- GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis.Scientific reports · 2019Article
- Differential Exosomic Proteomic Patterns and Their Influence in Resveratrol Sensitivities of Glioblastoma Cells.International journal of molecular sciences · 2019Article
- The role of G protein-coupled receptor kinases in the pathology of malignant tumors.Acta pharmacologica Sinica · 2018Review
- Reprogramming Medulloblastoma-Propagating Cells by a Combined Antagonism of Sonic Hedgehog and CXCR4.Cancer research · 2017Article
- Expression and Significances of G-Protein-Coupled Receptor Kinase 3 in Hepatocellular Carcinoma.Journal of Cancer · 2017Article
- Overexpression of GRK3, Promoting Tumor Proliferation, Is Predictive of Poor Prognosis in Colon Cancer.Disease markers · 2017Article
- G Protein-Coupled Receptor Kinases in the Inflammatory Response and Signaling.Advances in immunology · 2017Review
- G Protein Coupled Receptor Kinase 3 Regulates Breast Cancer Migration, Invasion, and Metastasis.PloS one · 2016Article
- Novel chemical library screen identifies naturally occurring plant products that specifically disrupt glioblastoma-endothelial cell interactions.Oncotarget · 2015Article
- Targeting brain tumor cAMP: the case for sex-specific therapeutics.Frontiers in pharmacology · 2015Article
- Molecular approaches for manipulating astrocytic signaling in vivo.Frontiers in cellular neuroscience · 2015Review
- G protein-coupled receptors as oncogenic signals in glioma: emerging therapeutic avenues.Neuroscience · 2014Review
- GRK3 is essential for metastatic cells and promotes prostate tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- PDE7B is a novel, prognostically significant mediator of glioblastoma growth whose expression is regulated by endothelial cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
G-protein-coupled receptor kinases (GRK) regulate the function of G-protein-coupled receptors (GPCR). Previously, we found that GPCR (CXCR4)-mediated astrocytoma growth was dependent upon abnormally sustained CXCR4 signaling and was correlated with decreased GRK-mediated receptor phosphorylation. As CXCR4 has also been implicated in the stimulation of high-grade glioma growth, we sought to determine whether dysregulation of GRK expression and/or function might also be present in high-grade gliomas. In an analysis of data from The Cancer Genome Atlas, we found that GRK3 expression is frequently decreased in glioblastoma (GBM) of the classical subtype, which possesses signature amplification or mutational activation of the epidermal growth factor (EGF) receptor. We tested the correlation between GRK3 expression and GBM subtypes, as well as the relationship between the activation of the EGF and other growth factor receptor pathways and GRK expression. In analyses of primary GBM tissue and RNA specimens, we found that GRK3 expression is correlated with established criteria for GBM subtyping including expression of EGF receptor, platelet-derived growth factor receptor (PDGFR)α, NF1, PTEN, CDKN2A, and neurofilament. We also found that established drivers of gliomagenesis, the EGF, PDGF, and TGF-β pathways, all regulate GRK expression. Coculture experiments, designed to mimic critical interactions between tumor and brain microvascular endothelial cells, showed that specifically increasing GRK3 expression reduced the trophic effect of endothelial cells on tumor cells. Together, these experiments show that GRK3 is a negative regulator of cell growth whose expression is preferentially reduced in GBM of the classical subtype as a consequence of activity in primary gliomagenic pathways.
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