ArticleCarcinogenesis2009
Regulation of the leucocyte chemoattractant receptor FPR in glioblastoma cells by cell differentiation.
Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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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
15 citing papers in PubMed, 23 citations in OpenAlex.
- Chemotherapy in pediatric brain tumor and the challenge of the blood-brain barrier.Cancer medicine · 2023Review
- Synthesis, biological evaluation, molecular modeling, and structural analysis of new pyrazole and pyrazolone derivatives as N-formyl peptide receptors agonists.Chemical biology & drug design · 2021Article
- The Contribution of Chemoattractant GPCRs, Formylpeptide Receptors, to Inflammation and Cancer.Frontiers in endocrinology · 2020Review
- High Glucose Promotes Human Glioblastoma Cell Growth by Increasing the Expression and Function of Chemoattractant and Growth Factor Receptors.Translational oncology · 2019Article
- Targeting Endothelial Barrier Dysfunction Caused by Circulating Bacterial and Mitochondrial N-Formyl Peptides With Deformylase.Frontiers in immunology · 2019Article
- Regulation of inflammation by members of the formyl-peptide receptor family.Journal of autoimmunity · 2017Review
- New development in studies of formyl-peptide receptors: critical roles in host defense.Journal of leukocyte biology · 2016Review
- Formylpeptide receptor 1 mediates the tumorigenicity of human hepatocellular carcinoma cells.Oncoimmunology · 2016Article
- The G-protein coupled chemoattractant receptor FPR2 promotes malignant phenotype of human colon cancer cells.American journal of cancer research · 2016Article
- Epigenetic therapy of cancer stem and progenitor cells by targeting DNA methylation machineries.World journal of stem cells · 2015Review
- Deregulated chromatin remodeling in the pathobiology of brain tumors.Neuromolecular medicine · 2013Review
- G protein-coupled receptor FPR1 as a pharmacologic target in inflammation and human glioblastoma.International immunopharmacology · 2012Review
- Annexin 1 released by necrotic human glioblastoma cells stimulates tumor cell growth through the formyl peptide receptor 1.The American journal of pathology · 2011Article
- HCV peptide (C5A), an amphipathic α-helical peptide of hepatitis virus C, is an activator of N-formyl peptide receptor in human phagocytes.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- The G-protein-coupled formylpeptide receptor FPR confers a more invasive phenotype on human glioblastoma cells.British journal of cancer · 2010Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
The G protein-coupled formylpeptide receptor (FPR), known to mediate phagocytic leucocyte chemotaxis in response to bacterial- and host-derived agonists, was expressed by tumor cells in specimens of surgically removed more highly malignant human gliomas. In human glioblastoma cell lines, FPR activation increased cell motility, tumorigenicity and production of angiogenic factors. In studies of the mechanistic basis for the selective expression of FPR in more highly malignant gliomas, we found that the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (Aza), while promoting the differentiation of human glioblastoma cells, downregulated FPR expression. Aza also reduced the global methylation levels in glioblastoma cells and activated the pathway of p53 tumor suppressor. Methylation-specific polymerase chain reaction revealed that Aza treatment of tumor cells reduced the methylation of p53 promoter, which was accompanied by increased expression of p53 gene and protein. In addition, overexpression of p53 in glioblastoma cells mimicked the effect of Aza treatment as shown by increased cell differentiation but reduction in FPR expression, the capacity of tumor sphere formation in soft agar and tumorigenesis in nude mice. Furthermore, Aza treatment or overexpression of the wild-type p53 in glioblastoma cells increased the binding of p53 to FPR promoter region shown by chromatin immunoprecipitation. These results indicate that increased methylation of p53 gene retains human glioblastoma cells at a more poorly differentiated phase associated with the aberrant expression of FPR as a tumor-promoting cell surface receptor.
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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.