Erucylphosphocholine-induced apoptosis in glioma cells: involvement of death receptor signalling and caspase activation

2002 | journal article. A publication with affiliation to the University of Göttingen.

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​Erucylphosphocholine-induced apoptosis in glioma cells: involvement of death receptor signalling and caspase activation​
Kugler, W.; Erdlenbruch, B.; Junemann, A.; Heinemann, D. E. H.; Eibl, H. & Lakomek, M.​ (2002) 
Journal of Neurochemistry82(5) pp. 1160​-1170​.​ DOI: https://doi.org/10.1046/j.1471-4159.2002.01034.x 

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Authors
Kugler, Wilfried; Erdlenbruch, Bernhard; Junemann, A.; Heinemann, D. E. H.; Eibl, H.; Lakomek, Max
Abstract
Erucylphosphocholine (ErPC) is a promising anti-neoplastic drug for the treatment of malignant brain tumours. It exerts strong anti-cancer activity in vivo and in vitro and induces apoptosis even in chemoresistant glioma cell lines. The purpose of this study was to expand on our previous observations on the potential mechanisms of ErPC-mediated apoptosis with a focus on death receptor activation and the caspase network. A172 and T98G glioma cells were treated with ErPC for up to 48 h. ErPC effects on the expression of the tumour necrosis factor (TNF) and TNF-related apoptosis-inducing ligand (TRAIL) receptor system, and on caspase activation were determined. ErPC had no effect on the expression of TNFalpha or TRAIL. Inhibition of the TNF or TRAIL signalling pathway with antagonistic antibodies or fusion proteins did not affect apoptosis induced by ErPC, and a dominant-negative FADD construct did not abolish ErPC-induced effects. Western blot analysis indicated that ErPC-triggered apoptosis resulted in a time-dependent processing of caspases-3, -7, -8 and -9 into their respective active subunits. Co-treatment of A172 cells with different caspase inhibitors prevented apoptosis but did not abrogate cell death. These data suggest that A172 cells might have an additional caspase-independent pathway that insures cell death and guarantees killing of those tumour cells whose caspase pathway is incomplete.
Issue Date
2002
Status
published
Publisher
Wiley-blackwell
Journal
Journal of Neurochemistry 
ISSN
0022-3042

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