Synergistic up-regulation of the myeloid-specific promoter for the macrophage colony-stimulating factor receptor by AML1 and the t(8;21) fusion protein may contribute to leukemogenesis.

Rhoades, K L; Hetherington, C J; Rowley, J D; Hiebert, S W; Nucifora, G; Tenen, D G; Zhang, D E

doi:10.1073/pnas.93.21.11895

Cited by 129Acute Myeloid Leukemia ResearchRetinoids in leukemia and cellular processesGenomics and Chromatin Dynamics

Synergistic up-regulation of the myeloid-specific promoter for the macrophage colony-stimulating factor receptor by AML1 and the t(8;21) fusion protein may contribute to leukemogenesis.

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Rhoades, K L, Hetherington, C J, Rowley, J D, Hiebert, S W, Nucifora, G, Tenen, D G, Zhang, D E·1996·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.93.21.11895PMC PMC38155

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Abstract

AML1 is involved in the (8;21) translocation, associated with acute myelogenous leukemia (AML)-type M2, which results in the production of the AML1-ETO fusion protein: the amino-terminal 177 amino acids of AML1 and the carboxyl-terminal 575 amino acids of ETO. The mechanism by which AML1-ETO accomplishes leukemic transformation is unknown; however, AML1-ETO interferes with AML1 transactivation of such AML1 targets as the T-cell receptor beta enhancer and the granulocyte-macrophage colony-stimulating factor promoter. Herein, we explored the effect of AML1-ETO on regulation of a myeloid-specific AML1 target, the macrophage colony-stimulating factor (M-CSF) receptor promoter. We found that AML1-ETO and AML1 work synergistically to transactivate the M-CSF receptor promoter, thus exhibiting a different activity than previously described. Truncation mutants within the ETO portion of AML1-ETO revealed the region of ETO necessary for the cooperativity between AML1 and AML1-ETO lies between amino acids 347 and 540. Endogenous M-CSF receptor expression was examined in Kasumi-1 cells, derived from a patient with AML-M2 t(8;21) and the promonocytic cell line U937. Kasumi-1 cells exhibited a significantly higher level of M-CSF receptor expression than U937 cells. Bone marrow from patients with AML-M2 t(8;21) also exhibited a higher level of expression of M-CSF receptor compared with normal controls. The upregulation of M-CSF receptor expression by AML1-ETO may contribute to the development of a leukemic state in these patients.

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Authors: Rhoades, K. L., Hetherington, C. J., Rowley, J. D., Hiebert, S. W., Nucifora, G., Tenen, D. G., & Zhang, D. E.
Affiliations: Division of Hematology/Oncology, Department of Medicine, Beth Israel Hospital, Boston, MA 02215, USA.
University of Chicago (US)
Harvard University (US)
ORCID: Rowley, J D
Hiebert, S W
Tenen, D G
Zhang, D E
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 1996-10-15
Volume: 93
Issue: 21
Pages: 11895-11900
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.93.21.11895
PMC: PMC38155
OpenAlex: W2074333479
Cited by: 129
References: 67
Citations by year: 2026: 1 · 2025: 2 · 2023: 1 · 2020: 1 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 3 · 2013: 1 · 2012: 6
FWCI: 4.33
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: U.S. Department of Energy (DE‐FG02‐)
National Institutes of Health (5f32ca068727-02)
National Cancer Institute (CA64140, CA68727-02, R01CA064140, CA1AI59589)
Topics: Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: AML1-ETO, RUNX1, acute myeloid leukemia, macrophage colony-stimulating factor receptor, transcriptional activation, synergistic gene regulation, Kasumi-1 cells, U937 cells, leukemogenesis
MeSH terms: RUNX1 Translocation Partner 1 Protein, Animals, Bone Marrow, Cell Line, Chlorocebus aethiops, Chromosomes, Human, Pair 21, Chromosomes, Human, Pair 8, DNA-Binding Proteins, Humans, Organ Specificity, Promoter Regions, Genetic, Proto-Oncogene Proteins, Transcription Factors, Translocation, Genetic, Tumor Cells, Cultured, Leukemia, Myeloid, Acute, Up-Regulation, Polymerase Chain Reaction, Receptor, Macrophage Colony-Stimulating Factor, DNA Primers, Core Binding Factor Alpha 2 Subunit

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Synergistic up-regulation of the myeloid-specific promoter for the macrophage colony-stimulating factor receptor by AML1 and the t(8;21) fusion protein may contribute to leukemogenesis.

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