Retinoids and myelomonocytic growth factors cooperatively activate RARΑ and induce human myeloid leukemia cell differentiation via MAP kinase pathways
Abstract
Use of all-trans-retinoic acid (ATRA) in combinatorial differentiation therapy of acute promyelocytic leukemia (APL) results in exceptional cure rates. However, potent cell differentiation effects of ATRA are so far largely restricted to this disease and long-term survival rates in non-APL acute myelogeneous leukemia (AML) remain unacceptably poor, requiring development of novel therapeutic strategies. We demonstrate here that myelomonocytic growth factors (granulocyte colony-stimulating factor [G-CSF] and/or granulocyte macrophage colony-stimulating factor [GM-CSF]) potentiate differentiation effects of ATRA in different AML cell lines and primary cells from patients with myeloid leukemia. The ligand-dependent activities of endogenous and transiently expressed retinoic acid receptor alpha (RARα) isoforms can be potentiated by G/GM-CSF in U-937 cells and correlate with increased expression of ATRA-inducible RARα2 isoform. Specific inhibitors of mitogen mitogen-activated protein kinase (MAPK) (MEK)-1/-2 or p38 extracellular signal-related kinase (ERK) kinase diminish the ATRA as well as ATRA and G/GM-CSF-induced activation of the RARα proteins and decreased the differentiation-induced decline in cell numbers. Our data demonstrate that acting, at least in part, via the MAP kinase pathways, myelomonocytic growth factors enhance ATRA-dependent activation of the RARα isoforms and maturation of myeloid leukemia cells. These results suggest that combinatorial use of these agents may be effective in differentiation therapy of AML. (Blood. 2005;105:341-349)
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The ligand-dependent activities of endogenous and transiently expressed RARα isoforms are enhanced by G/GM-CSF and correlate with an increased expression of ATRA inducible genes as well as leukaemic cell differentiation.
“The ligand-dependent activities of endogenous and transiently expressed RARα isoforms are enhanced by G/GM-CSF and correlate with an increased expression of ATRA inducible genes as well as leukaemic cell differentiation (Glasow et al, 2005).”
From Unlocking the potential of retinoic acid in anticancer therapy (2014) · cites this paper as Glasow et al, 2005
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- Authors
- Glasow, A., Prodromou, N., Xu, K., von Lindern, M., & Zelent, A.
- Affiliations
- Institute of Cancer Research (GB)
- From the section of Hematological Oncology, Institute of Cancer Research, London, United Kingdom; and the Department of Hematology, Erasmus Medical Center (MC), Rotterdam, The Netherlands.
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2005-01-01
- Volume
- 105
- Issue
- 1
- Pages
- 341-349
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2132791225
- Cited by
- 68
- References
- 54
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 1 · 2022: 3 · 2021: 4 · 2020: 3 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 3 · 2013: 2 · 2012: 6
- FWCI
- 1.90
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- all-trans retinoic acid, retinoic acid receptor alpha, acute myeloid leukemia, granulocyte colony-stimulating factor, GM-CSF, leukemia cell differentiation, MAPK signaling, differentiation therapy, U937 cells
- MeSH terms
- Retinoic Acid Receptor alpha, Animals, Cell Differentiation, Cell Division, Humans, Leukemia, Myeloid, Tretinoin, Tumor Cells, Cultured, Granulocyte-Macrophage Colony-Stimulating Factor, Granulocyte Colony-Stimulating Factor, Receptors, Retinoic Acid, Protein Isoforms, Response Elements, MAP Kinase Signaling System, Mice
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