Erufosine, a novel alkylphosphocholine, induces apoptosis in CLL through a caspase-dependent pathway

Abstract The alkylphosphocholine (APC) erufosine is a synthetic phospholipid analogue with antineoplastic activity. APC are known to interact with lipid metabolism and modulate cellular signaling pathways, particularly the phosphorylation of Akt. Here, in primary CLL cells induction of apoptosis was...

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Bibliographic Details
Published in:Leukemia research 2010-08, Vol.34 (8), p.1064-1069
Main Authors: Königs, Sonja Katharina, Pallasch, Christian Philipp, Lindner, Lars Hartwin, Schwamb, Janine, Schulz, Alexandra, Brinker, Reinhild, Claasen, Julia, Veldurthy, Aditya, Eibl, Hansjoerg, Hallek, Michael, Wendtner, Clemens-Martin
Format: Article
Language:English
Subjects:
Alkylphospholipid
Apoptosis
Apoptosis - drug effects
Blotting, Western
Caspases - metabolism
CLL
Erufosine
Hematology, Oncology and Palliative Medicine
Humans
Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy
Leukemia, Lymphocytic, Chronic, B-Cell - metabolism
Leukemia, Lymphocytic, Chronic, B-Cell - pathology
Organophosphates - pharmacology
Phospholipases A2 - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Quaternary Ammonium Compounds - pharmacology
Tumor Cells, Cultured
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Summary:Abstract The alkylphosphocholine (APC) erufosine is a synthetic phospholipid analogue with antineoplastic activity. APC are known to interact with lipid metabolism and modulate cellular signaling pathways, particularly the phosphorylation of Akt. Here, in primary CLL cells induction of apoptosis was detected with an IC50 of 22 μM whereas healthy donor PBMC were less sensitive towards erufosine. Treatment with erufosine caused dose-dependent cleavage of PARP, co-incubation with caspase inhibitor z-VAD almost completely abrogated the cytotoxic effect of erufosine indicating a caspase-dependent mechanism of erufosine. Erufosine was shown to induce apoptosis in primary CLL cells and merits further investigation regarding therapeutic options in CLL.
ISSN:0145-2126
1873-5835
DOI:10.1016/j.leukres.2009.12.003