Expression of CXC chemokine receptors 1-5 and their ligands in human glioma tissues: Role of CXCR4 and SDF1 in glioma cell proliferation and migration

被引:127
作者
Bajetto, Adriana
Barbieri, Federica
Dorcaratto, Alessandra
Barbero, Simone
Daga, Antonio
Porcile, Carola
Ravetti, Jean Louis
Zona, Gianluigi
Spaziante, Renato
Corte, Giorgio
Schettini, Gennaro
Florio, Tullio
机构
[1] Univ Genoa, Dept Oncol Biol & Genet, I-16132 Genoa, Italy
[2] Dept Surg Anaesthesiol & Transplants, Neurosurg Sect, Genoa, Italy
[3] Osped San Martino Genova, Sect Pathol, Genoa, Italy
[4] Univ Genoa, Dept Neurosci Ophthalmol & Genet, Neurosurg Sect, Genoa, Italy
[5] Natl Inst Canc Res, Expt Oncol Lab, Genoa, Italy
关键词
chemokine; CXCR4; SDF1; glioma; cell migration; cell proliferation;
D O I
10.1016/j.neuint.2006.03.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chemokines have been involved in cellular processes associated to malignant transformation such as proliferation, migration and angiogenesis. The expression of five CXC chemokine receptors and their main ligands was analysed by RT-PCR in 31 human astrocytic neoplasms. The mRNAs for all the receptors analysed were identified in a high percentage of tumours, while their ligands showed lower expression. CXCR4 and SDF1 were the most frequently mRNA identified (29/31 and 13/31 of the gliomas studied, respectively). Thus, we further analysed the cell localization of CXCR4 and SDF1 in immunohistochemistry experiments. We show a marked co-localization of CXCR4 and SDF1 in tumour cells, mainly evident in psudolpalisade and microcystic degeneration areas and in the vascular endothelium. In addition, hSDF1 alpha induced a significant increase of DNA synthesis in primary human glioblastoma cell cultures and chemotaxis in a glioblastoma cell line. These results provide evidence of the expression of multiple CXC chemokines and their receptors in brain tumours and that in particular CXCR4 and SDF1 sustain proliferation and migration of glioma cells to promote malignant progression. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:423 / 432
页数:10
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