Abstract
Integrin-dependent and -independent MMP-9 and uPAR signaling plays a key role in glioma cell migration and invasion. In this article, we comment on all the possible pathways and molecules associated with MMP-9- and uPAR-mediated glioma cell migration with a special emphasis on integrins, a family of cell adhesion molecules. Our recent research investigations highlighted the substantial benefit of silencing both MMP-9 and uPAR together compared with their individual treatments in glioma. Simultaneous knockdown of both MMP-9 and uPAR regulated a majority of the molecules associated with glioma cell migration and significantly reduced the migration potential of glioma cells. Our results point out that the bicistronic construct, which can simultaneously silence both MMP-9 and uPAR offers a great therapeutic potential and is worth developing as a new drug for treating GBM patients.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Actins / metabolism
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Brain Neoplasms / metabolism
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Brain Neoplasms / pathology
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Cell Movement*
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Extracellular Matrix / metabolism
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Gene Expression Regulation, Neoplastic*
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Gene Knockdown Techniques
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Glioma / genetics
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Glioma / metabolism
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Glioma / pathology*
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Humans
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Hyaluronan Receptors / genetics
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Hyaluronan Receptors / metabolism
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Integrin alpha Chains / genetics
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Integrin alpha Chains / metabolism
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Laminin / metabolism
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Matrix Metalloproteinase 9 / genetics
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Matrix Metalloproteinase 9 / metabolism*
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Protein Interaction Mapping
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RNA, Small Interfering / genetics
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RNA, Small Interfering / metabolism
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Receptors, Urokinase Plasminogen Activator / genetics
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Receptors, Urokinase Plasminogen Activator / metabolism*
Substances
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Actins
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CD44 protein, human
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Hyaluronan Receptors
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Integrin alpha Chains
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Laminin
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RNA, Small Interfering
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Receptors, Urokinase Plasminogen Activator
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MMP9 protein, human
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Matrix Metalloproteinase 9