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Cited by 90Cancer-related Molecular PathwaysRetinoids in leukemia and cellular processesCell death mechanisms and regulation

Staf50 is a novel p53 target gene conferring reduced clonogenic growth of leukemic U-937 cells

Obad, Susanna, Brunnström, Hans, Vallon-Christersson, Johan, Borg, Åke, Drott, Kristina, Gullberg, Urban·2004·Oncogene
DOI 10.1038/sj.onc.1207524
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Abstract

The tumor suppressor gene p53 is a transcription factor that mediates both cell cycle arrest and apoptosis. Interestingly, p53 also induces differentiation of a number of tissues, including leukemic cells. However, although p53-mediated differentiation of leukemic U-937 cells depends on the transcriptional activity of p53, a p53 target gene mediating differentiation has hitherto not been identified. To screen for novel p53 target genes in leukemic cells, a cDNA microarray analysis was performed with U-937-4/ptsp53 cells, expressing a temperature-sensitive p53 mutant. We report that transcription of the Staf50 (stimulated transacting factor of 50 kDa) gene is upregulated in response to wild-type p53 in U-937-4, K562 and MCF-7 cells. Staf50 was directly activated by p53, as determined by the independence of de novo protein synthesis. Moreover, while the proximal promoter of Staf50 was found not to be p53 responsive, a functional enhancer-like p53-response element in intron 1 of the Staf50 gene was identified that was also transactivated by the p53-family member p73. Direct binding of p53 to the response element was shown by electrophoretic mobility shift analysis. Ectopic expression of Staf50 in U-937 cells resulted in reduced clonogenic growth. Moreover, levels of endogenous Staf50 mRNA correlated to all-trans retinoic acid-induced differentiation of promyelocytic NB-4 and HL60 cells, suggesting that Staf50 could be involved in proliferation and/or differentiation of leukemic cells.

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Crossref · 10.1038/sj.onc.1207524

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  • Members of the TRIM protein family, such as PML (TRIM19) and TRIM22, are transcriptionally activated by p53 and have been shown to alter the p53 response.

    “Members of the TRIM protein family, such as PML (TRIM19)222 and TRIM22,223 are transcriptionally activated by p53 and have been shown to alter the p53 response.224”

    From Census and evaluation of p53 target genes (2017) · cites this paper as [223]

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Authors
Obad, S., Brunnström, H., Vallon-Christersson, J., Borg, Å., Drott, K., & Gullberg, U.
Affiliations
Lund University (SE)
Corresponding author
Gullberg, Urban
ORCID
Venue
Oncogene
Publisher
Springer Science and Business Media LLC
Published
2004-04-05
Volume
23
Issue
23
Pages
4050-4059
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
DOI
10.1038/sj.onc.1207524
OpenAlex
W1975228908
Cited by
90
References
48
Citations by year
2026: 2 · 2025: 3 · 2024: 3 · 2023: 4 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 2 · 2018: 6 · 2017: 4 · 2016: 2 · 2015: 5 · 2014: 4 · 2013: 9 · 2012: 7
FWCI
2.24
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Oncogene (publishedVersion)
  • PubMed (publishedVersion)
  • Lund University Publications (Lund University) (submittedVersion)
Funders
  • Lunds Universitet
  • Gunnar Nilssons Cancerstiftelse
  • Knut och Alice Wallenbergs Stiftelse
  • Vetenskapsrådet
  • Greta och Johan Kocks stiftelser
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
p53 target genes, p53, leukemia cell differentiation, U937 cells, p73, p53 response elements, clonogenic growth, retinoic acid differentiation, promyelocytic leukemia, transcriptional activation, temperature-sensitive p53 mutant
MeSH terms
Tripartite Motif Proteins, Tumor Protein p73, Binding Sites, Breast Neoplasms, DNA-Binding Proteins, Gene Expression Regulation, Humans, Nuclear Proteins, Promoter Regions, Genetic, Repressor Proteins, RNA, Messenger, Transcription Factors, Tretinoin, Minor Histocompatibility Antigens, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Interferon-alpha, U937 Cells, Amino Acid Motifs, Myeloid Cells, Tumor Suppressor Proteins

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