The combination of Steel factor and GM-CSF blocks apoptosis induced by retinoic acid and upregulates AP-1 in a human growth factor-dependent cell line

M. Horie, H. E. Broxmeyer

Research output: Contribution to journalArticle

19 Scopus citations


The effects of hematopoietic growth factors were examined on the cellular action of retinoic acid (RA) using the human factor-dependent cell line, MO7e. Treatment of cells with Steel factor (SLF) plus granulocyte-maclophage colony-stimulating factor (GM-CSF) synergistically stimulated cell proliferation compared to that with each factor alone. This synergism was even greater in the presence of RA than in its absence. Treatment of cells with RA resulted in apoptotic cell death associated with internucleosomal DNA fragmentation in the presence of either SLF or GM-CSF. RA-induced apoptosis and DNA fragmentation were completely blocked by treating cells with SLF plus GM-CSF. Northern analysis showed that the inhibition of RA effects on MO7e cells by SLF plus GM-CSF treatment occurred without modulation of expression of RA receptor-α (RAR-α) gene. Furthermore, a higher amount of AP-1 complex was detected by electrophoretic mobility shift assays in a nuclear extract prepared from cells treated with SLF plus GM-CSF compared to those treated with each factor alone, while the level of RAR-complex remained similar in cells treated with SLF and/or GM-CSF. These data suggest an interaction in signaling pathways among different types of receptors that might be associated with the AP-1 complex.

Original languageEnglish (US)
Pages (from-to)168-173
Number of pages6
JournalExperimental Hematology
Issue number2
StatePublished - Jan 1 1995



  • AP-1
  • Apoptosis
  • GM-CSF
  • Retinoic acid
  • Steel factor

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Genetics
  • Hematology
  • Oncology
  • Transplantation

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