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Progression of the myeloid differentiation program is dominant to
transforming growth factor-beta 1-induced apoptosis in M1 myeloid leukemic
cells
M Selvakumaran, JC Reed, D Liebermann and B Hoffman
Fels Institute for Cancer Research and Molecular Biology, Temple University
School of Medicine, Philadelphia, PA 19140.
Hematopoiesis is a profound example of cell homeostasis that is regulated
throughout life. This process requires the participation of many factors,
including positive and negative regulators of growth and differentiation,
that determine survival, growth stimulation, differentiation, functional
activation, and programmed cell death. Understanding the effects of
multiple stimuli on specific cells at the molecular and cellular level is
crucial towards understanding how the population of blood cells maintains a
homeostatic state. Two appropriate stimuli for analysis, both of which are
found in bone marrow, are differentiation-inducing cytokines, which induce
terminal differentiation associated with growth arrest, ultimately
culminating in programmed cell death, and transforming growth factor-beta 1
(TGF- beta 1), which induces rapid growth arrest and apoptosis of
hematopoietic cells. Previously, we have shown, using M1 myeloblastic
leukemic cells as a model system, that differentiation-inducing cytokines
induce terminal differentiation associated with growth arrest and, only
after 5 to 7 days, apoptosis, whereas TGF-beta 1 induces rapid growth
arrest and apoptosis. In this report, we show that M1 myeloid leukemic
cells treated concomitantly with the differentiation inducer interleukin-6
and TGF-beta 1 undergo terminal differentiation, in which modulators of the
MyD118 gene product, previously shown to be a positive regulator of
TGF-beta 1-induced apoptosis, are implicated to play a role in protecting
the cells from TGF-beta 1-induced apoptosis. Furthermore, using M1 cell
variants blocked at different stages after induction of differentiation,
including M1myb and M1myc, as well as conditionally blocked M1mycer, it has
been shown that the dominance of interleukin-6 to TGF-beta 1-induced
apoptosis is dependent on the progression of the differentiation program.
Further studies with M1 and the genetically engineered M1 cell variants
will be instrumental towards molecularly dissecting the interaction of
hematopoietic differentiation with a variety of apoptotic pathways.
Volume 84,
Issue 4,
pp. 1036-1042,
08/15/1994
Copyright © 1994 by The American Society of Hematology
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