TITLE

Mechanisms of Resistance of Human Glioma Cells to Apo2 Ligand/TNF-Related Apoptosis-Inducing Ligand

AUTHOR(S)
Rieger, Johannes; Frank, Brigitte; Weller, Michael; Wick, Wolfgang
PUB. DATE
July 2007
SOURCE
Cellular Physiology & Biochemistry (Karger AG);2007, Vol. 20 Issue 1-4, p023
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Many tumor cells are resistant to Apo2L/TRAIL-induced apoptosis in the absence of inhibitors of protein synthesis. Apo2L/TRAIL, in addition to induction of apoptosis, may therefore also activate survival pathways. Methods: Here we investigated whether such survival pathways mediate resistance to Apo2L.0-induced apoptosis in human glioma cells. Results: Apo2L.0 induced the phosphorylation of ERK1/2, but not of Akt. This effect was unaffected by caspase inhibition. Inhibitors of protein synthesis, PI3 kinase, ERK kinase, NF-κB or casein kinase 2 sensitized for Apo2L.0-induced apoptosis to a different extent in a panel of human malignant glioma cell lines. However, none of the sensitizers overcame resistance mediated by ectopic expression of the viral caspase 8 inhibitor, crm-A. Primary glioma cultures were almost completely resistant to Apo2L.0-induced cell death even in the presence of the inhibitors. Caspase-8 was expressed in these cells whereas only weak expression of DR5 was detected. Transient expression of DR5 conferred sensitivity to Apo2L.0. Conclusion: These data challenge the view that specific cell lines harbour specific mechanisms of resistance to Apo2L/TRAIL. Weak expression of DR5 in primary glioma might limit the therapeutic application of Apo2L/TRAIL in human glioblastoma patients. Copyright © 2007 S. Karger AG, Basel
ACCESSION #
25449235

 

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