Epigalocatechin-3-gallate (EGCG) downregulates PEA15 and thereby augments TRAIL-mediated apoptosis in malignant glioma |
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| Authors: | Siegelin M D Habel A Gaiser T |
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| Affiliation: | Department of Neuropathology, University Hospital Heidelberg, Im Neuenheimer Feld 220, 69120 Heidelberg, Germany. markus.siegelin@med.uni-heidelberg.de |
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| Abstract: | EGCG is a flavonoid that exhibited therapeutic activity in cancer. In this study three glioblastoma cell lines (U87, A172 and U251) were treated with EGCG, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or the combination of both. Treatment with subtoxic doses of EGCG in combination with TRAIL induces rapid apoptosis in TRAIL-resistant glioma cells, suggesting that this combined treatment may offer an attractive strategy for treating gliomas. EGCG treatment down-regulated phosphoprotein-enriched in astrocytes (PEA15) through an Akt (PKB)-dependent mechanism. In addition, over-expression of PEA15 attenuated cytotoxicity induced by the combination of EGCG and TRAIL. In summary, PEA15 is a key regulator in TRAIL-EGCG-mediated cell death in malignant glioma. |
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| Keywords: | TRAIL, tumor necrosis factor-related apoptosis-inducing ligand IAPs, inhibitor of apoptosis proteins PEA15, phosphoprotein-enriched in astrocytes EGCG, epigallocatechin-3-gallate DISC, death-inducing signalling complex ph-Akt, phosphorylated Akt PKB, protein kinase B |
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