Background & objective: Chemoattractant receptors participate in essential pathophysiologic processes, including inflammation, wound healing, human immunodeficiency virus infection, and most interestingly in the progression of malignant tumor. This study was to explore the functional expression of formylpeptide receptor (FPR) in human glioblastoma cell line U87.
Methods: The expression of FPR in U87 and FPR small interfering RNA (siRNA)-transfected U87 cells (FPR-siRNA-U87 cells) was detected with indirect immunofluorescent staining by confocal laser scanning microscopy. FPR was activated by its ligand formy-Met-Leu-Phe (fMLF). Cell proliferation was assessed by MTT assay. The production of vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) was measured by ELISA, and IL-8 mRNA was assessed by reverse transcription-polymerase chain reaction (RT-PCR).
Results: FPR was expressed on U87 cells, but not on FPR-siRNA-U87 cells. After activation of FPR by fMLF, the proliferation of U87 cells was enhanced markedly (P<0.05), but that of FPR-siRNA-U87 cells had no obvious change (P>0.05). fMLF (100 nmol/L) elicited a time-dependent increase in the secretion of IL-8 and VEGF. When stimulated with 100 nmol/L fMLF for 36 h, the protein levels of VEGF and IL-8 were significantly higher in stimulated U87 cells than in control cells [(3.13+/-0.23) ng/ml vs. (2.55+/-0.25) ng/ml, P<0.05û (7.54+/-0.53) ng/ml vs. (4.02+/-0.09) ng/ml, P<0.05], but those in FPR-siRNA-U87 cells had no obvious change; the mRNA level of IL-8 was significantly increased in U87 cells, but not changed in FPR-siRNA-U87 cells.
Conclusion: Activating FPR can promote the proliferation of U87 cells and enhance the production of angiogenic factors.