G-CSF RECEPTOR-MEDIATED UP-REGULATION OF C-FOS BUT NOT C-RAF MESSENGER-RNA EXPRESSION IN MYELOID CELLS

Granulocyte colony stimulating factor (G-CSF) regulates survival, prol iferation, and differentiation of myeloid precursor cells. One of the signaling mechanisms for the G-CSF receptor (G-CSF-R) involves the act ivation of Ras/MAP kinase (MEK) pathway. Since Raf is an important, co mmon link between Ras and MEK in the Ras-Raf-MEK cascade, we studied t he expression of c-raf mRNA in G-CSF-treated myeloid precursor cell li nes-NFS-60 and HL-60. G-CSF did not alter c-raf mRNA expression in the se cells up to 24 h, but induced a transient up-regulation of c-fos mR NA expression between 15-60 min post-treatment. Our results show that G-CSF triggers a de novo induction of c-fos but not c-raf mRNA, and su ggests that G-CSF-R-mediated activation of Ras/MEK pathway may involve post-transcriptional mechanisms of Raf regulation.