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Phorbol ester-stimulated phosphorylation of PU.1: association with leukemic cell growth inhibition
Open accessAbstract
PU.1, a member of the ets transcription factor family, has been previously shown to be necessary for tetradecanoylphorbol-13 acetate (TPA)-induced U937 leukemic cell maturation. We examined the effects of TPA on PU.1 content and PU.1 DNA binding activity in U937 cells. Unstimulated cells expressed PU.1 mRNA transcripts and TPA did not increase these levels. However, TPA treatment induced phosphorylation of PU.1. Gel-shift analysis using a labeled PU.1 oligomer showed that TPA induced a unique PU.1 binding activity. This binding activity was phosphorylation-dependent, as indicated by the ability of phosphatase treatment to abolish its detection. The PU.1 binding activity was generated at TPA-13 concentrations stimulating growth arrest and was blocked by the PKC inhibitor GF109203X, which antagonized TPA-induced growth inhibition. Bryostatin 1, another protein kinase C activator, induced only a modest degree of U937 growth inhibition and antagonized TPA-stimulated growth arrest. Bryostatin 1 was unable to induce this TPA-generated PU.1 binding activity. High bryostatin 1 concentrations inhibited generation of this TPA-induced band shift. These data suggest that TPA-induced growth inhibition is associated with phosphorylation of PU.1 and generation of a unique PU.1 binding activity.
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“PMA is known induce monocyte-macrophage differentiation in U937 cells through PU.1 upregulation (43)”
From FBW7 Inhibits Myeloid Differentiation in Acute Myeloid Leukemia via GSK3-Dependent Ubiquitination of PU.1 (2021) · cites this paper as [43]
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“We were not able to detect tyrosine-phosphorylated PU.1 by using this approach, consistent with previous results (28).”
From PU.1, Interferon Regulatory Factor (IRF) 2, and the Interferon Consensus Sequence-binding Protein (ICSBP/IRF8) Cooperate to Activate NF1 Transcription in Differentiating Myeloid Cells (2007) · cites this paper as [28]
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References 38 · Cited by 58
Metadata
- Authors
- Carey, J., Posekany, K., deVente, J., Pettit, G., & Ways, D.
- Affiliations
- Cancer Research Institute (US)
- Department of Medicine, East Carolina University School of Medicine, Greenville, NC 27858, USA.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 1996-05-15
- Volume
- 87
- Issue
- 10
- Pages
- 4316-4324
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2415933643
- Cited by
- 58
- References
- 38
- Citations by year
- 2023: 1 · 2020: 1 · 2018: 2 · 2017: 2 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 2
- FWCI
- 2.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (CA-43823)
- 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 › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
- Keywords
- PU.1, phorbol myristate acetate, protein kinase C, protein phosphorylation, U937 cells, ETS transcription factors, DNA-binding activity, bryostatin 1, growth arrest
- MeSH terms
- Proto-Oncogene Protein Spi-1, Base Sequence, Cell Differentiation, Cell Division, DNA, Neoplasm, Enhancer Elements, Genetic, Enzyme Inhibitors, Humans, Indoles, Lactones, Maleimides, Molecular Sequence Data, Neoplasm Proteins, Phosphorylation, Protein Binding, Protein Kinase C, Protein Processing, Post-Translational, Proto-Oncogene Proteins, Proto-Oncogenes, RNA, Messenger, RNA, Neoplasm, Tetradecanoylphorbol Acetate, Transcription Factors, Transcription, Genetic, Tumor Cells, Cultured, Trans-Activators, Gene Expression Regulation, Leukemic, Lymphoma, Large B-Cell, Diffuse, Macrolides, Bryostatins
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