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Vol. 12, No. 7, pp. 968-981, April 1, 1998
B activation in
Bcr-Abl-mediated transformation
1 Lineberger Comprehensive Cancer Center,
2 Curriculum in Genetics and Molecular Biology, and
3 Department of Biology, University of North Carolina at
Chapel Hill, Chapel Hill, North Carolina 27599 USA;
4 Department of Pharmacology and Cancer Biology, Duke
University Medical Center, Durham, North Carolina 27710 USA
Bcr-Abl is a chimeric oncoprotein that is strongly implicated in
acute lymphoblastic (ALL) and chronic myelogenous leukemias (CML). This
deregulated tyrosine kinase selectively causes hematopoietic disorders
resembling human leukemias in animal models and transforms fibroblasts
and hematopoietic cells in culture. Bcr-Abl also protects cells from
death induced on cytokine deprivation or exposure to DNA damaging
agents. In addition, the antiapoptotic function of Bcr-Abl is thought
to play a necessary role in hematopoietic transformation and
potentially in leukemogenesis. The transcription factor NF-
B has
been identified recently as an inhibitor of apoptosis and as a
potential regulator of cellular transformation. This study shows that
expression of Bcr-Abl leads to activation of NF-B-dependent transcription by causing nuclear translocation of NF-B as well as by
increasing the transactivation function of the RelA/p65 subunit of NF-B. Importantly, this activation is dependent on the
tyrosine kinase activity of Bcr-Abl and partially requires Ras. The
ability of Bcr-Abl to protect cytokine-dependent 32D myeloid cells
from death induced by cytokine deprivation or DNA damage does not,
however, require functional NF-B. However, using a super-repressor
form of IB
, we show that NF-B is required for
Bcr-Abl-mediated tumorigenicity in nude mice and for transformation of
primary bone marrow cells. This study implicates NF-B as an important component of Bcr-Abl signaling. NF-B-regulated genes, therefore, likely play a role in transformation by Bcr-Abl and thus in
Bcr-Abl-associated human leukemias.
[Key Words:
Bcr-Abl; NF-B; IB; tumorigenesis; apoptosis]
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