TNF-alpha-induced growth suppression of CD34+ myeloid leukemic cell lines signals through TNF receptor type I and is associated with NF-kappa B activation

J Immunol. 1999 Sep 15;163(6):3106-15.

Abstract

Conflicting results have been reported regarding the effect of TNF-alpha on the growth of human primitive hemopoietic cells. In this study, we have examined the effect of TNF-alpha 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-alpha 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-alpha-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-alpha 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-alpha treatment. Neutralizing anti-TNF receptor type I (TNFR-I; p55) Ab almost completely reversed TNF-alpha-induced growth inhibition in both liquid and soft agar cultures, whereas anti-TNFR-II (p75) Ab had only a marginal effect. TNF-alpha rapidly induced marked activation of nuclear transcription factor NF-kappa 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-alpha is incapable of inducing activation of the mitogen-activated protein kinase pathway in these leukemic cell lines.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • ADP-ribosyl Cyclase
  • ADP-ribosyl Cyclase 1
  • Antigens, CD / physiology*
  • Antigens, CD34 / biosynthesis*
  • Antigens, Differentiation / biosynthesis
  • Antineoplastic Agents / pharmacology
  • Apoptosis / immunology
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Clone Cells
  • Enzyme Activation / immunology
  • Growth Inhibitors / physiology*
  • Humans
  • Leukemia, Erythroblastic, Acute / immunology*
  • Leukemia, Erythroblastic, Acute / metabolism
  • Leukemia, Erythroblastic, Acute / pathology*
  • Membrane Glycoproteins
  • NAD+ Nucleosidase / biosynthesis
  • NF-kappa B / metabolism*
  • Necrosis
  • Receptors, Tumor Necrosis Factor / physiology*
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Signal Transduction / immunology*
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / physiology*

Substances

  • Antigens, CD
  • Antigens, CD34
  • Antigens, Differentiation
  • Antineoplastic Agents
  • Growth Inhibitors
  • Membrane Glycoproteins
  • NF-kappa B
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Tumor Necrosis Factor-alpha
  • Calcium-Calmodulin-Dependent Protein Kinases
  • ADP-ribosyl Cyclase
  • CD38 protein, human
  • NAD+ Nucleosidase
  • ADP-ribosyl Cyclase 1