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Blood, Vol. 94 No. 10 (November 15), 1999:
pp. 3583-3592
Liposomal ET-18-OCH3 Induces Cytochrome c-Mediated
Apoptosis Independently of CD95 (APO-1/Fas) Signaling
Olivier Cuvillier,
Eric Mayhew,
Andrew S. Janoff, and
Sarah Spiegel
From the Department of Biochemistry and Molecular Biology, Georgetown
University Medical Center, Washington, DC; and The Liposome Co, Inc,
Princeton, NJ.
ELL-12, a liposome formulation of the ether-lipid
1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine
(ET-18-OCH3), is a nonmyelosuppressive antiproliferative
agent that is more effective and less toxic than the ether lipid itself
in tumor model systems. We found that ELL-12 induced apoptosis in
Jurkat, H9, and U-937 cells that was preceded by activation of
executioner caspases. In addition, ELL-12 triggered release of
cytochrome c from mitochondria to the cytoplasm before
caspase-9 activation. Apoptosis, activation of caspases, and cytochrome
c release were blocked by Bcl-xL overexpression in
Jurkat T cells, suggesting a critical role for mitochondria in
ELL-12-triggered cell death. Furthermore, ELL-12 had no effect on
expression of CD95 ligand, and inhibition of the Fas signaling pathway
with antagonistic anti-CD95 antibody did not affect apoptosis induced
by ELL-12. Hence, ELL-12 could be a promising adjunct for the treatment
of tumors in addition to myelosuppressive chemotherapeutic drugs and/or
those that use the CD95-ligand/receptor system to trigger apoptosis.
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