Glycosaminoglycans modulate C6 glioma cell adhesion to extracellular matrix components and alter cell proliferation and cell migration
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
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Data(s) |
26/08/2013
26/08/2013
01/08/2005
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Resumo |
Abstract Background Adhesion to extracellular matrix (ECM) components has been implicated in the proliferative and invasive properties of tumor cells. We investigated the ability of C6 glioma cells to attach to ECM components in vitro and described the regulatory role of glycosaminoglycans (GAGs) on their adhesion to the substrate, proliferation and migration. Results ECM proteins (type IV collagen, laminin and fibronectin) stimulate rat C6 glioma cell line adhesion in vitro, in a dose-dependent manner. The higher adhesion values were achieved with type IV collagen. Exogenous heparin or chondroitin sulfate impaired, in a dose-dependent manner the attachment of C6 glioma cell line to laminin and fibronectin, but not to type IV collagen. Dextran sulfate did not affect C6 adhesion to any ECM protein analyzed, indicating a specific role of GAGs in mediating glioma adhesion to laminin and fibronectin. GAGs and dextran sulfate did not induce C6 glioma detachment from any tested substrate suggesting specific effect in the initial step of cell adhesion. Furthermore, heparin and chondroitin sulfate impaired C6 cells proliferation on fibronectin, but not on type IV collagen or laminin. In contrast, both GAGs stimulate the glioma migration on laminin without effect on type IV collagen or fibronectin. Conclusion The results suggest that GAGs and proteoglycans regulate glioma cell adhesion to ECM proteins in specific manner leading to cell proliferation or cell migration, according to the ECM composition, thus modulating tumor cell properties. We thank Professor Vivaldo Moura Neto, Universidade Federal do Rio de Janeiro, Brazil, for providing C6 cells. Research supported by CAPES and CNPq. We thank Professor Vivaldo Moura Neto, Universidade Federal do Rio de Janeiro, Brazil, for providing C6 cells. Research supported by CAPES and CNPq. |
Identificador |
1471-2121 http://www.producao.usp.br/handle/BDPI/32741 10.1186/1471-2121-6-31 |
Idioma(s) |
eng |
Relação |
BMC Cell Biology |
Direitos |
openAccess de Aguiar et al; licensee BioMed Central Ltd. - This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
Tipo |
article original article |