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- W2258906453 abstract "In the course of studying the role of chemoattractant receptors in tumor growth and metastasis, we discovered that highly malignant human glioblastoma and anaplastic astrocytoma specimens were stained positively for the formylpeptide receptor FPR, which is normally expressed in myeloid cells and accounts for their chemotaxis and activation induced by bacterial peptides. Screening of human glioma cell lines revealed that FPR was expressed only in glioma cells with a more highly malignant phenotype. FPR expressed in glioblastoma cell lines mediates cell chemotaxis, proliferation and production of VEGF, in response to agonistic ligands released by necrotic tumor cells. Furthermore, FPR in glioblastoma cells transactivates the receptor for epidermal growth factor (EGFR) by a signal transduction pathway that increases the phosphorylation of a selected tyrosine residue in EGFR. This transactivation of EGFR by FPR accounts for part of the function of FPR in tumor cells. Depletion of FPR or EGFR in tumor cells by small interference (si) RNA each reduces the capacity of the tumor cells to form actively growing tumors in nude mice, while depletion of both receptors completely abolishes the tumorigenicity of glioblastoma cells. Thus, FPR aberrantly expressed in human glioblastoma cells by responding to agonistic ligands produced in the tumor microenvironment cooperates with EGFR to promote rapid tumor progression. These results suggest important molecular targets for the design of novel anti-glioblastoma therapeutics." @default.
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- W2258906453 date "2008-03-01" @default.
- W2258906453 modified "2023-09-23" @default.
- W2258906453 title "The formylpeptide receptor FPR exploits the function of the epidermal growth factor receptor to promote the progression of glioblastoma" @default.
- W2258906453 doi "https://doi.org/10.1096/fasebj.22.1_supplement.665.2" @default.
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