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Involvement of ecto-5′-nucleotidase/CD73 in U138MG glioma cell adhesion

Involvement of ecto-5′-nucleotidase/CD73 in U138MG glioma cell adhesion Glioblastoma multiform is the most common and aggressive type of brain tumor. The overexpression of ecto-5′-nucleotidase/CD73 (ecto-5′-NT/CD73), an adhesion molecule and the main enzymatic source of extracellular adenosine, has been reported in tumor cells, and it is emerging as a component of glioma progression. Here, we evaluated the involvement of ecto-5′-NT/CD73 in cell adhesion through its interaction with different components of the extracellular matrix in the human U138MG glioma cell line. The results indicated that adenosine induced an increase in glioma cell adhesion. The treatment of glioma cells with adenosine receptor antagonists, APCP (α,β-methylene ADP) and dipyridamole prevented the adenosine effect, indicating the participation of extracellular and intracellular signaling pathways in cell adhesion mediated by adenosine. The ECM protein laminin (lam) and chondroitin sulfate (ChS) modulated the ecto-5′-NT/CD73 activity and glioma adhesion in a parallel manner, suggesting the involvement of purinergic signaling in the effects mediated by the extracellular matrix. Taken together, these results suggest that ecto-5′-NT/CD73, an important producer of extracellular adenosine, may modulate glioma cell adhesion and tumor cell–extracellular matrix interactions. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular and Cellular Biochemistry Springer Journals

Involvement of ecto-5′-nucleotidase/CD73 in U138MG glioma cell adhesion

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References (47)

Publisher
Springer Journals
Copyright
Copyright © 2011 by Springer Science+Business Media, LLC.
Subject
Life Sciences; Medical Biochemistry; Oncology; Cardiology; Biochemistry, general
ISSN
0300-8177
eISSN
1573-4919
DOI
10.1007/s11010-011-1025-9
pmid
21858682
Publisher site
See Article on Publisher Site

Abstract

Glioblastoma multiform is the most common and aggressive type of brain tumor. The overexpression of ecto-5′-nucleotidase/CD73 (ecto-5′-NT/CD73), an adhesion molecule and the main enzymatic source of extracellular adenosine, has been reported in tumor cells, and it is emerging as a component of glioma progression. Here, we evaluated the involvement of ecto-5′-NT/CD73 in cell adhesion through its interaction with different components of the extracellular matrix in the human U138MG glioma cell line. The results indicated that adenosine induced an increase in glioma cell adhesion. The treatment of glioma cells with adenosine receptor antagonists, APCP (α,β-methylene ADP) and dipyridamole prevented the adenosine effect, indicating the participation of extracellular and intracellular signaling pathways in cell adhesion mediated by adenosine. The ECM protein laminin (lam) and chondroitin sulfate (ChS) modulated the ecto-5′-NT/CD73 activity and glioma adhesion in a parallel manner, suggesting the involvement of purinergic signaling in the effects mediated by the extracellular matrix. Taken together, these results suggest that ecto-5′-NT/CD73, an important producer of extracellular adenosine, may modulate glioma cell adhesion and tumor cell–extracellular matrix interactions.

Journal

Molecular and Cellular BiochemistrySpringer Journals

Published: Aug 21, 2011

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