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Cited by 45Retinoids in leukemia and cellular processesAcute Myeloid Leukemia ResearchGenomics and Chromatin Dynamics

PML-Retinoic Acid Receptor α Inhibits PML IV Enhancement of PU.1-Induced C/EBPε Expression in Myeloid Differentiation

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Yoshida, Hitoshi, Ichikawa, Hitoshi, Tagata, Yusuke, Katsumoto, Takuo, Ohnishi, Kazunori, Akao, Yukihiro, Naoe, Tomoki, Pandolfi, Pier Paolo +1 more·2007·Molecular and Cellular Biology
DOI 10.1128/mcb.02422-06PMC PMC1952121
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Abstract

PML and PU.1 play important roles in myeloid differentiation. PML-deficient mice have an impaired capacity for terminal maturation of their myeloid precursor cells. This finding has been explained, at least in part, by the lack of PML action to modulate retinoic acid-differentiating activities. In this study, we found that C/EBPepsilon expression is reduced in PML-deficient mice. We showed that PU.1 directly activates the transcription of the C/EBPepsilon gene that is essential for granulocytic differentiation. The type IV isoform of PML interacted with PU.1, promoted its association with p300, and then enhanced PU.1-induced transcription and granulocytic differentiation. In contrast to PML IV, the leukemia-associated PML-retinoic acid receptor alpha fusion protein dissociated the PU.1/PML IV/p300 complex and inhibited PU.1-induced transcription. These results suggest a novel pathogenic mechanism of the PML-retinoic acid receptor alpha fusion protein in acute promyelocytic leukemia.

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  • Moderate PU.1 inhibition is common in AML patients.

    “yet moderate PU.1 inhibition is common in AML patients”

    From Minimal PU.1 reduction induces a preleukemic state and promotes development of acute myeloid leukemia (2015) · cites this paper as [17]

    The Results report that PML-RARA suppressed PU.1-induced expression and granulocytic differentiation in experimental cells, and the Discussion links reduced PU.1 activity to leukemia in mice. The paper does not establish that moderate PU.1 inhibition is common among AML patients; neither its experimental setting nor its evidence supports that frequency claim. (LLM, conf=0.84)

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Cited by

Sorted by citations

Authors
Yoshida, H., Ichikawa, H., Tagata, Y., Katsumoto, T., Ohnishi, K., Akao, Y., Naoe, T., Pandolfi, P. P., & Kitabayashi, I.
Affiliations
  • National Cancer Center Research Institute (JP)
  • Hamamatsu University School of Medicine (JP)
  • Department of Genetic Diagnosis, Gifu International Institute of Biotechnology, Kakamigahara, Japan
  • Nagoya University (JP)
  • Memorial Sloan Kettering Cancer Center (US)
Corresponding author
Yoshida, Hitoshi
ORCID
Venue
Molecular and Cellular Biology
Publisher
Informa UK Limited
Published
2007-08-01
Volume
27
Issue
16
Pages
5819-5834
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
DOI
10.1128/mcb.02422-06
PMC
PMC1952121
OpenAlex
W2010643205
Cited by
45
References
4
Citations by year
2023: 1 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 1 · 2017: 2 · 2016: 3 · 2015: 2 · 2014: 3 · 2013: 7 · 2012: 1
FWCI
1.72
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)
  • Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
Funders
Institut National de la Santé et de la Recherche Médicale
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 › Genomics and Chromatin Dynamics
Keywords
PML, PU.1, C/EBPε, myeloid differentiation, granulocytic differentiation, P300, transcriptional activation, PML isoforms, acute promyelocytic leukemia
MeSH terms
Promyelocytic Leukemia Protein, Proto-Oncogene Protein Spi-1, Animals, Base Sequence, Cell Differentiation, HeLa Cells, Humans, Molecular Sequence Data, Neoplasm Proteins, Nuclear Proteins, Protein Binding, Proto-Oncogene Proteins, Structure-Activity Relationship, Transcription Factors, Transcription, Genetic, Oncogene Proteins, Fusion, Trans-Activators, Protein Isoforms, Myeloid Cells, CCAAT-Enhancer-Binding Proteins, Tumor Suppressor Proteins, Myelopoiesis, NIH 3T3 Cells, Granulocyte Precursor Cells, E1A-Associated p300 Protein, Mice

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