ArticleJournal of neuro-oncology2015
Microenvironment involved in FPR1 expression by human glioblastomas.
Article in Journal of neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Assessing the potential of bacterial signal peptides for radiopharmaceutical applications.Scientific reports · 2025Article
- Energy metabolism-related GLUD1 contributes to favorable clinical outcomes of IDH-mutant glioma.BMC neurology · 2024Article
- SIRT3 Regulates the ROS-FPR1/HIF-1α Axis under Hypoxic Conditions to Influence Lung Cancer Progression.Cell biochemistry and biophysics · 2023Article
- Bidirectional Functional Effects ofMicroorganisms · 2022Review
- Application of small molecule FPR1 antagonists in the treatment of cancers.Scientific reports · 2020Article
- Bioinformatic Profiling of Prognosis-Related Genes in Malignant Glioma Microenvironment.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- FPR1 mediates the tumorigenicity of human cervical cancer cells.Cancer management and research · 2018Article
- Anti-glioma Activity of Dapsone and Its Enhancement by Synthetic Chemical Modification.Neurochemical research · 2017Article
- The urokinase receptor-derived cyclic peptide [SRSRY] suppresses neovascularization and intravasation of osteosarcoma and chondrosarcoma cells.Oncotarget · 2016Article
- Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Formyl peptide receptor 1 (FPR1) activity in U87 glioblastoma (GBM) cells contributes to tumor cell motility. The present study aimed to evaluate the FPR1 expression in human GBM, the possibility to elicit agonist induced FPR1 activation of GBM cells and inhibit this activation with chemotaxis inhibitory protein of Staphylococcus aureus (CHIPS). Immunohistochemistry was used to assess FPR1 expression in GBM patient samples, which was present in all 178 samples. Also FPR1 mRNA levels measured with quantitative PCR, could be detected in all 25 GBM patient samples tested. Activation of FPR1 in U87 cells, as measured by human mitochondrial-derived agonists, increased calcium mobilization, AKT and ERK1/2 phosphorylation, and ligand-induced migration. Inhibition of all responses could be achieved with CHIPS. Eight early passage human Groningen Glioma (GG) cell lines, isolated from primary GBM tissue were screened for the presence of FPR1. FPR1 mRNA and protein expression as well as receptor activation could not be detected in any of these early passage GG cell lines. However FPR1 was present in ex vivo tumors formed by the same GG cell lines after being implanted in mouse brains. FPR1 is highly expressed in human GBM specimens, it can be activated by human mitochondrial-derived agonists in U87 and inhibited with CHIPS. FPR1 cannot be detected in early passage GG cell lines in vitro, however when engrafted in the mouse brain these cells show FPR1 expression. These results suggest a role of the brain microenvironment in FPR1 expression in GBM.
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