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Review
. 2008 Jul-Sep;2(3):202-7.
doi: 10.4161/cam.2.3.6320. Epub 2008 Jul 21.

Role of hyaluronan in glioma invasion

Jong Bae Park  1 , Hee-Jin Kwak, Seung-Hoon Lee
Affiliations
Review

Role of hyaluronan in glioma invasion

Jong Bae Park et al. Cell Adh Migr. 2008 Jul-Sep.

Abstract

Gliomas are the most common primary intracranial tumors. Their distinct ability to infiltrate into the extracellular matrix (ECM) of the brain makes it impossible to treat these tumors using surgery and radiation therapy. A number of different studies have suggested that hyaluronan (HA), the principal glycosaminoglycan (GAG) in the ECM of the brain, is the critical factor for glioma invasion. HA-induced glioma invasion was driven by two important molecular events: matrix metalloproteinase (MMP) secretion and up-regulation of cell migration. MMP secretion was triggered by HA-induced focal adhesion kinase (FAK) activation, which transmits its signal through ERK activation and nuclear factor kappa B (NF-kappaB) translocation. Another important molecular event is osteopontin (OPN) expression. OPN expression by AKT activation triggers cell migration. These results suggest that HA-induced glioma invasion is tightly regulated by signaling mechanisms, and a detailed understanding of this molecular mechanism will provide important clues for glioma treatment.

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Figures

Figure 1
Figure 1
Inhibition mechanism of emodin on HA-induced glioma invasion and motility. HA induced the invasion of glioma cells by the induction of MMP-9 through the RaS/FAK/ERK 1, 2 activation. In addition, NFκB translocation by FAK activation is also important for the MMP-9 expression. PTEN can effectively modulate the expression of MMP-9 by the dephosphorylation of FAK. HA induced the motililty of glioma cells by the induction of OPN through the PI3K/AKT/mTOR pathway. PTEN can effectively modulate the expression of OPN, and induced OPN contributes to HA-induced cell migration in glioma cells. Emodin suppresses HA-induced MMP-9 and OPN expression through the inhibition of FAK, and AKT activation. Emodin as a protein tyrosine kinase inhibitor can block protein kinases which are important for the HA-induced glioma invasion and motility.
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