Contribution of the formylpeptide receptor FPR to the rapid growth of malignant human glioblastoma.

ZHOU, Y.; BIAN, X.; LE, Y.; GONG, W.; ZHANG, X.; WANG, L.; IRIBARREN P; SALCEDO, R.; HOWARD, O. M. Z.; FARRAR, W.

Journal of the National Cancer Institute

Año: 2005 vol. 97 p. 823 - 823

0027-8874

p class="abstract">BACKGROUND: The formylpeptide receptor (FPR) is a G-protein-coupled receptor (GPCR) that mediates chemotaxis of phagocytic leukocytes induced by bacterial peptide N-formyl-methionyl-leucyl-phenylalanine (fMLF). We previously showed that selected human glioma cell lines also express functional FPR. We therefore investigated the relationship between FPR expression and the biologic behavior of glioma cells. METHODS: Expression and function of FPR in the human glioblastoma cell line U-87 were examined by reverse transcription-polymerase chain reaction (RT-PCR) and chemotaxis assays, respectively. FPR protein expression was detected in specimens from 33 human primary gliomas by immunohistochemistry. FPR short interfering (si) RNA was used to block FPR expression in U-87 cells. Cell proliferation was assessed by measuring DNA synthesis. Xenograft tumor formation and growth were measured in nude mice. Endogenous FPR agonist activity released by necrotic tumor cells was ass