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BCR-ABL Delays Apoptosis Upstream of Procaspase-3 Activation
Laurence Dubrez,
Béatrice Eymin,
Olivier Sordet,
Nathalie Droin,
Ali G. Turhan, and
Eric Solary
From the Department of Biology and Therapy of Cancer, INSERM CJF
94-08, Faculty of Medicine, Dijon, and INSERM U 362, IGR, Villejuif,
France.
The p210bcr-abl protein was shown to inhibit apoptosis
induced by DNA damaging agents. Apoptotic DNA fragmentation is delayed
in the bcr-abl+ K562 and KCL-22 compared with the
bcr-abl U937 and HL-60 cell lines when treated
with etoposide concentrations that induce similar DNA damage in the
four cell lines. By the use of a cell-free system, we show that nuclei
from untreated cells that express p210bcr-abl remain
sensitive to apoptotic DNA fragmentation induced by triton-soluble extracts from p210bcr-abl cells treated with etoposide.
In the four tested cell lines, apoptotic DNA fragmentation is
associated with a decreased expression of procaspase-3
(CPP32/Yama/apopain) and its cleavage into a p17 active fragment,
whereas the long isoform of procaspase-2 (ICH-1L) remains unchanged and
the poly(adenosine diphosphate-ribose)polymerase protein is cleaved.
These events are delayed in bcr-abl+ compared
with bcr-abl cell lines. The role of
p210bcr-abl in this delay is confirmed by comparing the
effect of etoposide on the granulocyte-macrophage colony-stimulating
factor (GM-CSF)-dependent UT7 cells and the
bcr-abl-transfected GM-CSF-independent UT7/9 clone. We
conclude that the cytosolic pathway that leads to apoptotic DNA
fragmentation in etoposide-treated leukemic cells is delayed upstream
of procaspase-3-mediated events in bcr-abl+ cell
lines.
Blood, Vol. 91 No. 7 (April 1), 1998:
pp. 2415-2422
© 1998 by The American Society of Hematology.
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