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-Induced Growth Suppression of CD34+ Myeloid Leukemic Cell Lines Signals Through TNF Receptor Type I and Is Associated with NF-
B Activation1
,§
*
Division of Medical Oncology and Hematology, Department of Internal Medicine,
Department of Biochemistry and Molecular Biology, and
Department of Anatomy, University South Florida, and
§
Molecular Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612
Conflicting results have been reported regarding the effect of
TNF-
on the growth of human primitive hemopoietic cells. In this
study, we have examined the effect of TNF- on the proliferation of
several CD34+/CD38+ (KG-1, TF-1) and
CD34+/CD38- (KG-1a, TF-1a) myeloid leukemic
progenitor cell lines. Our data show that TNF- markedly inhibits the
growth of these cells in both liquid and soft agar cultures. Addition
of GM-CSF or IL-3 does not prevent TNF--induced growth inhibition.
Flow cytometry analyses of propidium iodide-stained cells demonstrated
cell death of all four cell lines, as judged by the presence of cells
with hypodiploid DNA content after exposure of cells to TNF- for 4
days. Annexin V assays detected apoptosis in TF-1, but not in TF-1a,
KG-1, and KG-1a cells in terms of translocation of phosphatidylserine
shortly after TNF- treatment. Neutralizing anti-TNF receptor
type I (TNFR-I; p55) Ab almost completely reversed TNF--induced
growth inhibition in both liquid and soft agar cultures, whereas
anti-TNFR-II (p75) Ab had only a marginal effect. TNF- rapidly
induced marked activation of nuclear transcription factor NF-
B in
all 4 cell lines. The majority of this effect was abolished by the type
I receptor Ab, whereas the type II receptor neutralizing Ab had no
effect. Our data also show that TNF- is incapable of inducing
activation of the mitogen-activated protein kinase pathway in these
leukemic cell lines.
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