Down-modulation of Bis reduces the invasive ability of glioma cells induced by TPA, through NF-κB mediated activation of MMP-9
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Bcl-2 interacting cell death suppressor (Bis) has been shown tohave anti-apoptotic and anti-stress functions. Recently, increasedBis expression was reported to correlate with gliomaaggressiveness. Here, we investigated the effect of Bis knockdownon the acquisition of the invasive phenotype of A172glioma cells, induced by 12-O-Tetradecanoylphorbol- 3-acetate(TPA), using a Transwell assay. Bis knockdown resulted in asignificant decrease in the migration and invasion of A172cells. Furthermore, Bis knockdown notably decreased TPAinducedmatrix metalloproteinase-9 (MMP-9) activity andmRNA expression, as measured by zymography and quantitativereal time PCR, respectively. A luciferase reporter assayindicated that Bis suppression significantly down-regulatedNF-κB-driven transcription. Finally, we demonstrated that therapid phosphorylation and subsequent degradation of IκB-αinduced by TPA was remarkably delayed by Bis knockdown. These results suggest that Bis regulates the invasive ability ofglioma cells elicited by TPA, by modulating NF-κB activation,and subsequent induction of MMP-9 mRNA.
Abstract
Bcl-2 interacting cell death suppressor (Bis) has been shown tohave anti-apoptotic and anti-stress functions. Recently, increasedBis expression was reported to correlate with gliomaaggressiveness. Here, we investigated the effect of Bis knockdownon the acquisition of the invasive phenotype of A172glioma cells, induced by 12-O-Tetradecanoylphorbol- 3-acetate(TPA), using a Transwell assay. Bis knockdown resulted in asignificant decrease in the migration and invasion of A172cells. Furthermore, Bis knockdown notably decreased TPAinducedmatrix metalloproteinase-9 (MMP-9) activity andmRNA expression, as measured by zymography and quantitativereal time PCR, respectively. A luciferase reporter assayindicated that Bis suppression significantly down-regulatedNF-κB-driven transcription. Finally, we demonstrated that therapid phosphorylation and subsequent degradation of IκB-αinduced by TPA was remarkably delayed by Bis knockdown. These results suggest that Bis regulates the invasive ability ofglioma cells elicited by TPA, by modulating NF-κB activation,and subsequent induction of MMP-9 mRNA.
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