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Cited by 263Acute Myeloid Leukemia ResearchRetinoids in leukemia and cellular processesGenomics and Chromatin Dynamics

c-Myc Is a Critical Target for C/EBPα in Granulopoiesis

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Johansen, Lisa M., Iwama, Atsushi, Lodie, Tracey A., Sasaki, Koichi, Felsher, Dean W., Golub, Todd R., Tenen, Daniel G.·2001·Molecular and Cellular Biology
DOI 10.1128/mcb.21.11.3789-3806.2001PMC PMC87031
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Abstract

CCAAT/enhancer binding protein alpha (C/EBPalpha) is an integral factor in the granulocytic developmental pathway, as myeloblasts from C/EBPalpha-null mice exhibit an early block in differentiation. Since mice deficient for known C/EBPalpha target genes do not exhibit the same block in granulocyte maturation, we sought to identify additional C/EBPalpha target genes essential for myeloid cell development. To identify such genes, we used both representational difference analysis and oligonucleotide array analysis with RNA derived from a C/EBPalpha-inducible myeloid cell line. From each of these independent screens, we identified c-Myc as a C/EBPalpha negatively regulated gene. We mapped an E2F binding site in the c-Myc promoter as the cis-acting element critical for C/EBPalpha negative regulation. The identification of c-Myc as a C/EBPalpha target gene is intriguing, as it has been previously shown that down-regulation of c-Myc can induce myeloid differentiation. Here we show that stable expression of c-Myc from an exogenous promoter not responsive to C/EBPalpha-mediated down-regulation forces myeloblasts to remain in an undifferentiated state. Therefore, C/EBPalpha negative regulation of c-Myc is critical for allowing early myeloid precursors to enter a differentiation pathway. This is the first report to demonstrate that C/EBPalpha directly affects the level of c-Myc expression and, thus, the decision of myeloid blasts to enter into the granulocytic differentiation pathway.

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  • G-CSF-mediated activation of STAT3 induces granulocytic progenitor proliferation through transcriptional upregulation of C/EBPβ and c-Myc.

    “granulocyte cell-stimulating factor–mediated activation of STAT3 induces granulocytic progenitor proliferation through transcriptional upregulation of CCAAT/enhancer-binding protein (C/EBP)β and c-Myc”

    From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Johansen et al., 2001

    The Discussion (page unavailable) says that maintaining c-Myc expression keeps myeloblasts proliferative, supporting c-Myc’s role in proliferation. It does not establish that G-CSF activates STAT3 to transcriptionally upregulate C/EBPβ and c-Myc; the mechanism it examines is C/EBPα-mediated downregulation of c-Myc. (LLM, conf=0.82)

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Authors
Johansen, L. M., Iwama, A., Lodie, T. A., Sasaki, K., Felsher, D. W., Golub, T. R., & Tenen, D. G.
Affiliations
  • Harvard University (US)
  • University of Tsukuba (JP)
  • Stanford Medicine (US)
Corresponding author
Tenen, Daniel G.
ORCID
Venue
Molecular and Cellular Biology
Publisher
Informa UK Limited
Published
2001-06
Volume
21
Issue
11
Pages
3789-3806
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
DOI
10.1128/mcb.21.11.3789-3806.2001
PMC
PMC87031
OpenAlex
W2127632559
Cited by
263
References
7
Citations by year
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FWCI
10.04
Type
journal article
Language
en
Open access
Licence
journals.asm.org/non-commercial-tdm-license (tdm)
Locations
  • Molecular and Cellular Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL056745, HL56745)
  • National Institute of Diabetes and Digestive and Kidney Diseases (F32DK09892, F32DK009892)
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
c-Myc, C/EBPα, granulopoiesis, granulocytic differentiation, myeloid differentiation, transcriptional repression, E2F binding sites, c-myc promoter, myeloblasts, myeloid cell development
MeSH terms
Animals, Binding Sites, Carrier Proteins, Cell Differentiation, Cell Line, Chlorocebus aethiops, DNA-Binding Proteins, Gene Expression Regulation, Granulocytes, Humans, Neutrophils, Promoter Regions, Genetic, Transcription Factors, Tumor Cells, Cultured, Proto-Oncogene Proteins c-myc, Cell Cycle Proteins, COS Cells, U937 Cells, CCAAT-Enhancer-Binding Protein-alpha, Transcription Factor DP1, E2F Transcription Factors, Retinoblastoma-Binding Protein 1

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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