Journal
PEDIATRIC RESEARCH
Volume 57, Issue 1, Pages 63-66Publisher
NATURE PUBLISHING GROUP
DOI: 10.1203/01.PDR.0000147729.55592.2C
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Funding
- NATIONAL CANCER INSTITUTE [R55CA068221, R29CA068221] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL075826] Funding Source: NIH RePORTER
- NCI NIH HHS [CA68221] Funding Source: Medline
- NHLBI NIH HHS [HL 75826] Funding Source: Medline
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Granulocyte colony-stimulating factor (G-CSF) is a growth factor that regulates the production and function of neutrophils. G-CSF has been used to treat neutropenia in neonates, pediatric cancer patients, and patients undergoing stem cell transplantation. The regulation of transcription factors mediating G-CSF activity has not been well characterized. The goal of this study was to examine the regulation of the ETS binding protein, Friend leukemia integration site 1 (Fli-1), in myeloid cells treated with G-CSF. Fli-1 has oncogenic properties in humans and mice, and plays a role in vascular and hematopoietic cell development. We previously reported that Fli-1 and the serum response factor bind at adjacent sites within the serum response element-1 of the early growth response gene-1 promoter in the murine myeloid leukemic cell line, NFS60. We also identified that Fli-1 DNA binding increased in G-CSF-treated cells compared with untreated cells. To determine whether the change in binding activity is due to increased Fli-1 transcription or protein stability, we examined endogenous Fli-1 expression in G-CSF-treated or -untreated NFS60 cells. Our results demonstrated that levels of Fli-1 protein, but not RNA, were higher in extracts from cells treated with G-CSF. The increase in Fli-1 protein was also dependent on protein synthesis. Finally, we showed that the half-life of Fli-1 is prolonged in G-CSF-treated cells compared with control-treated cells. These results suggest that G-CSF induces stabilization of Fli-1 protein in myeloid cells, thus proposing a novel mechanism by which hematopoietic growth factors regulate transcription factors.
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