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Erucylphosphocholine-induced apoptosis in chemoresistant glioblastoma cell lines: Involvement of caspase activation and mitochondrial alterations

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Eibl,  H.
Research Group of Phospholipids, MPI for biophysical chemistry, Max Planck Society;

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Citation

Jendrossek, V., Kugler, W., Erdlenbruch, B., Eibl, H., Lang, F., & Lakomek, M. (2001). Erucylphosphocholine-induced apoptosis in chemoresistant glioblastoma cell lines: Involvement of caspase activation and mitochondrial alterations. Anticancer Research, 21(5), 3389-3396. Retrieved from http://www.scopus.com/record/display.url?eid=2-s2.0-0035569921&origin=inward&txGid=1ue0Na80aifVxLDLJhHMWBd%3a32#.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-F535-4
Abstract
Intrinsic chemoresistance constitutes a major problem in the therapy of malignant gliomas. In vitro experiments with four astrocytoma/glioblastoma (AC/GBM) cell lines revealed that the chemoresistance of two cell lines, A 172 and T98G, to cisplatin and etoposide was due to resistance to drug-induced apoptosis. In contrast, all the AC/GBM cell lines tested were sensitive to treatment with the lipophilic ether lipid erucylphosphocholine, ErPC. ErPC-induced apoptosis was independent of wild-type p53- signaling and triggering of the CD95/CD95 ligand (CD95L) system. Inhibition of protein and RNA synthesis by cycloheximide and actinomycin D did not abrogate ErPC-induced apoptosis. However, expression of members of the bcl-2 protein family was modulated during ErPC treatment. Activation of caspase 3 and mitochondrial alterations were central to ErPC- induced apoptosis. We conclude that ErPC-induced activation of the mitochondrial pathway enables cell death in the chemoresistant AC/GBM cells.