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[Cancer Research 63, 1969-1974, April 15, 2003]
© 2003 American Association for Cancer Research

Tumor Biology

Stromal Cell-derived Factor 1{alpha} Stimulates Human Glioblastoma Cell Growth through the Activation of Both Extracellular Signal-regulated Kinases 1/2 and Akt1

Simone Barbero, Rudy Bonavia, Adriana Bajetto, Carola Porcile, Paolo Pirani, Jean Louis Ravetti, Gian Luigi Zona, Renato Spaziante, Tullio Florio and Gennaro Schettini2

Pharmacology and Neuroscience, National Institute for Cancer Research c/o Advanced Biotechnology Center, Genoa, Italy [S. B., R. B., A. B., C. P., P. P., G. S.]; Section of Pharmacology, Department of Oncology, Biology and Genetic, University of Genoa, Genoa, Italy [S. B., R. B., A. B., C. P., T. F., G. S.]; Service of Pathology Hospital San Martino, Genoa, Italy [J. L. R.]; and Division of Neurosurgery, Department of Neurology and of the Vision Sciences, University of Genoa, Genoa, Italy [G. L. Z., R. S.]

In this paper, we describe the role of chemokine receptor CXCR4 activation by its natural ligand, the chemokine stromal cell-derived factor (SDF-1) (CXCL12), in glioblastoma cell growth in vitro. We show that both CXC chemokine receptor 4 (CXCR4) and SDF-1 mRNA are expressed in several human glioblastoma multiforme tumor tissues and in two human glioblastoma cell lines, U87-MG and DBTRG-05MG. These cells are able to secrete SDF-1 under basal conditions, and the rate of secretion is highly increased after lipopolysaccharide or 1% fetal bovine serum treatment. Exogenous SDF-1{alpha} induces proliferation in a dose-dependent manner in both cell lines. Moreover, we observed that SDF-1{alpha}-dependent proliferation is correlated with phosphorylation and activation of both extracellular signal-regulated kinases 1/2 and Akt and that these kinases are independently involved in glioblastoma cell proliferation. The role of CXCR4 stimulation in glioblastoma cell growth is further demonstrated by the ability of human monoclonal CXCR4 antibody (clone 12G5) to inhibit the SDF-1{alpha}-induced proliferation as well as the proliferation induced by SDF-1-releasing treatments (lipopolysaccharide and 1% fetal bovine serum). These data support a role for SDF-1{alpha} in the regulation of glioblastoma growth in vitro, likely through an autocrine/paracrine mechanism.




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