Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
Vol. 13, No. 8, 2014, pp. 1327-1332
Bioline Code: pr14182
Full paper language: English
Document type: Research Article
Document available free of charge
Tropical Journal of Pharmaceutical Research, Vol. 13, No. 8, 2014, pp. 1327-1332
© Copyright 2014 - Tropical Journal of Pharmaceutical Research
Synthetic Polypeptide Derived from Viral Macrophage Inflammatory Protein II Inhibit VEGF Production of Human Glioma U87 Cells through SDF-1α/CXCR4-Mediated AKT Signaling Pathway|
Xu, Bo; Tian, Peng; An, Gui-Jie; Liu, Sha; Li, Xiu-Ying; Sun, Han-Xiao; Zhou, Jing-Gung; Ding, Qing & Wei, Pi-Jin
Purpose: To evaluate the effect of synthetic polypeptide (N15P) derived from viral macrophage
inflammatory protein II (vMIP-II) on the secretion of vascular endothelial growth factor (VEGF) as well as
investigate the signaling pathways involved in stromal cell-derived factor-1α (SDF-1α)/CXC Chemokin
Receptor 4 (CXCR4) axis-induced VEGF in glioblastoma U87 cells.
Methods: Glioblastoma U87 cells were exposed to SDF-1α, N15P with various concentrations. The
expression of CXCR4, SDF-1α and VEGF mRNA were assessed by RT-PCR, while expression level of
VEGF was tested by ELISA and protein kinase B (Akt) phosphorylation detected by Western blot.
Results: The results showed that CXCR4, SDF-1α, VEGF are expressed in human glioblastoma U87
cell lines. SDF-1α caused a dose-dependent sensitivity of cell proliferation with a maximum effect at 15
μmole/ml, while N15P decreased cell viability in U87 cells in a dose-dependent manner. SDF-1α
stimulated the activation of VEGF, and N15P inhibited the activation of VEGF with or without SDF-1α
stimulation. VEGF production in U87 cells was associated with Akt pathway. These changes in
intracellular processes were blocked by N15P in a dose-dependent manner.
Conclusion: The results suggest that N15P suppress SDF-1α/CXCR4 Mediated VEGF production
through Akt signaling pathway and this may be a potent therapeutic strategy in glioblastoma.
Viral macrophage; Inflammatory protein II; Glioblastoma; CXC chemokin receptor 4; Stromal cell-derived factor-1α; Protein kinase B
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