Two pathways of apoptosis induced with all-trans retinoic acid and etoposide in the myeloid cell line P39

Exp Hematol. 1999 Aug;27(8):1322-9. doi: 10.1016/s0301-472x(99)00066-1.

Abstract

P39/Tsugane is a myelomonocytoid cell line derived from a patient with myelodysplastic syndrome (MDS). The cells readily undergo apoptosis in response to various agents, and the cell line has been suggested as a useful model to study apoptosis in MDS. The aims of the present study were to assess differentiation and apoptosis induced with all-trans retinoic acid (ATRA) and etoposide, to characterize the mode of apoptosis in these two model systems, and to assess the influence of granulocyte colony-stimulating factor (G-CSF), which in combination with erythropoietin has been shown to inhibit apoptosis in MDS. ATRA induced differentiation and apoptosis in a concentration- and time-dependent manner. Differentiated cells were partially rescued (by 50%) from apoptosis with G-CSF. Etoposide induced apoptosis in a concentration- and time-dependent manner, but no signs of preceding maturation or G-CSF rescue were detected. ATRA- and etoposide-induced apoptosis were both mediated through the caspase pathway and were partially blocked with the general caspase inhibitor zVAD-fmk. Simultaneous treatment with G-CSF and zVAD-fmk additively blocked ATRA-induced apoptosis. However, the two pathways differed in terms of substrate cleavage during apoptosis. ATRA-induced apoptosis caused actin cleavage, which was not affected by G-CSF, and Bcl-2 downregulation. Etoposide induced a caspase-dependent cleavage of Bcl-2, while actin remained intact. The Fas system did not seem to play a major role in any of these apoptotic pathways. Our results may provide new tools to study the mechanisms of apoptosis in MDS.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Acute Disease
  • Amino Acid Chloromethyl Ketones / pharmacology
  • Antibodies, Monoclonal / pharmacology
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Blast Crisis / etiology
  • Blast Crisis / pathology
  • Caspase Inhibitors
  • Caspases / physiology
  • Cell Differentiation / drug effects
  • Cysteine Proteinase Inhibitors / pharmacology
  • Cytoskeleton / drug effects
  • Cytoskeleton / metabolism
  • Erythropoietin / pharmacology
  • Etoposide / pharmacology*
  • Granulocyte Colony-Stimulating Factor / pharmacology
  • Humans
  • Leukemia, Myeloid / etiology
  • Leukemia, Myeloid / pathology*
  • Myelodysplastic Syndromes / complications
  • Myelodysplastic Syndromes / pathology*
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / physiology
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology
  • Tretinoin / pharmacology*
  • Tumor Cells, Cultured / drug effects
  • fas Receptor / immunology

Substances

  • Actins
  • Amino Acid Chloromethyl Ketones
  • Antibodies, Monoclonal
  • Caspase Inhibitors
  • Cysteine Proteinase Inhibitors
  • Neoplasm Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
  • fas Receptor
  • Erythropoietin
  • Granulocyte Colony-Stimulating Factor
  • Tretinoin
  • Etoposide
  • Caspases