Effect of resveratrol on matrix metalloproteinase-2 (MMP-2) and Secreted Protein Acidic and Rich in Cysteine (SPARC) on human cultured glioblastoma cells
Introduction. – Glioblastoma is a highly malignant brain tumor with a high-invasive phenotype, so the prognosis is unfavorable, even in response to multidisciplinary treatment strategies. Obviously, therefore, a better therapeutic strategy is needed. Resveratrol has been reported to be one of the mo...
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Published in | Biomedicine & pharmacotherapy Vol. 59; no. 7; pp. 359 - 364 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
France
Elsevier SAS
01.08.2005
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Subjects | |
Online Access | Get full text |
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Summary: | Introduction. –
Glioblastoma is a highly malignant brain tumor with a high-invasive phenotype, so the prognosis is unfavorable, even in response to multidisciplinary treatment strategies. Obviously, therefore, a better therapeutic strategy is needed. Resveratrol has been reported to be one of the most potent chemopreventive agents inhibiting the cellular processes associated with tumor development, including initiation, promotion, and progression.
Materials and methods. –
In this study we used RT-PCR, western blot and SDS-zymography to investigate the effect of resveratrol on the expression of genes and proteins involved in the extracellular matrix remodeling associated with tumor invasion in human cultured glioblastoma cells treated for 24, 48 and 72 h. We analyzed the expression of matrix metalloproteinase-2 (MMP-2), the main mediator of glioblastoma invasiveness, and the Secreted Protein Acidic and Rich in Cysteine (SPARC), involved in the regulation of cell–matrix interactions.
Results. –
Our results show a dose-related decrease of MMP-2 mRNA and protein levels 72 h after resveratrol treatment, and lower SPARC gene and protein expression 72 h after resveratrol treatment. This indicates that resveratrol may influence the two major factors in the ECM remodeling occurring with tumor invasion, suggesting it may have uses as a therapeutic agent for brain tumors. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0753-3322 1950-6007 |
DOI: | 10.1016/j.biopha.2005.06.001 |