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Special Focus: Glioma Therapy

Role of hyaluronan in glioma invasion

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Pages 202-207 | Received 02 Apr 2008, Accepted 21 May 2008, Published online: 01 Jul 2008

Figures & data

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.

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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