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BCR-ABL maintains resistance of chronic myelogenous leukemia cells to
apoptotic cell death [published erratum appears in Blood 1994 Jun
15;83(12):3835]
A McGahon, R Bissonnette, M Schmitt, KM Cotter, DR Green and TG Cotter
Department of Biology, St Patrick's College, Kildare, Ireland.
Apoptosis is the major form of cell death associated with the action of
chemotherapeutic agents on tumor cells, and therefore the expression of
genes that interfere with apoptosis can have important consequences for the
efficacy of therapeutic approaches. Here we show that K562, a chronic
myelogenous leukemia (CML) cell line expressing the BCR-ABL fusion protein,
are resistant to the induction of apoptosis by a number of agents and
conditions. Antisense oligodeoxynucleotides corresponding to the
translation start of bcr downregulate bcr-abl protein in these cells and
render them susceptible to induction of apoptosis by chemotherapeutic
agents or serum deprivation. Expression of a temperature sensitive v-Abl
protein reverses the effects of the antisense oligonucleotides, such that
the cells remain resistant to apoptosis at the permissive temperature.
These data indicate that bcr- abl acts as an anti-apoptosis gene in CML
cells and suggests that the effect is dependent on the abl kinase activity
in this chimeric protein. Inhibition of bcr-abl to render CML cells
susceptible to apoptosis can be combined with therapeutic drugs and/or
treatment capable of inducing apoptosis to provide an effective strategy
for elimination of these cells.
Volume 83,
Issue 5,
pp. 1179-1187,
03/01/1994
Copyright © 1994 by The American Society of Hematology
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