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J Biol Chem, Vol. 274, Issue 7, 3927-3930, February 12, 1999
Activity Is Necessary for Bcr-Abl-mediated
Resistance to Drug-induced Apoptosis
,¶
From the K562 chronic myelogenous leukemia cells are
highly resistant to chemotherapeutic drugs, such as taxol, that induce
cell death by apoptosis. This resistance is mediated by the chimeric
tyrosine kinase oncogene Bcr-Abl. However, little is known about the
mechanism by which Bcr-Abl protects K562 cells from apoptosis. We
recently demonstrated that expression of PKC Sealy Center for Oncology and Hematology and
the Departments of ¶ Pharmacology and Human Biological
Chemistry and Genetics, University of Texas Medical Branch, Galveston,
Texas 77555-1048 and the § Garvan Institute of Medical
Research, Darlinghurst,
Sydney, New South Wales 2010, Australia
is necessary for the
resistance of K562 cells to taxol-induced apoptosis (Murray, N. R., and Fields, A. P. (1997) J. Biol. Chem. 272, 27521-27524). We now demonstrate that treatment of K562 cells with
taxol leads to sustained activation of PKC. In contrast,
Bcr-Abl-negative HL60 myeloid leukemia cells, which are sensitive to
taxol-induced apoptosis, do not exhibit sustained PKC
activation in response to taxol. Treatment of K562 cells with
tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks taxol-induced
PKC activation and sensitizes these cells to taxol-induced apoptosis, indicating that PKC is a relevant downstream target of
Bcr-Abl-mediated resistance. Furthermore, expression of constitutively active PKC by adenovirus-mediated gene transfer rescues
AG957-treated K562 cells from taxol-induced apoptosis. Taken together,
these results demonstrate that both Bcr-Abl and PKC activity are
necessary for apoptotic resistance in K562 cells. Furthermore, they
identify PKC as a critical downstream target of Bcr-Abl that is
sufficient to mediate the anti-apoptotic effects of Bcr-Abl.
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