Cited by 147Cancer-related Molecular PathwaysAcute Myeloid Leukemia ResearchGenomics and Chromatin Dynamics

Induction of Sp1-p53 DNA-binding heterocomplexes during granulocyte/macrophage colony-stimulating factor-dependent proliferation in human erythroleukemia cell line TF-1.

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Borellini, F., Glazer, R.I.·1993·Journal of Biological Chemistry

Abstract

The involvement of Sp1 in regulating cell proliferation in myeloid leukemia cells was determined by measuring the levels and DNA binding activity of Sp1 in TF-1 cells, a human erythroleukemia cell line dependent on granulocyte/macrophage colony-stimulating factor (GM-CSF) for viability and cell growth. DNA binding of Sp1 to a specific double-stranded oligodeoxynucleotide was increased markedly in a dose-dependent manner in proliferating cells in response to GM-CSF compared with growth-arrested or apoptotic cells. Competition experiments and mobility shift interference assays with antibodies against Sp1 as well as wild-type or mutant p53 indicated that GM-CSF-inducible DNA-binding complexes contained both Sp1 and p53 and that these heterocomplexes bound to both p53- and Sp1-binding sequences with high affinity. Immunoprecipitation of nuclear extracts with a p53 antibody indicated that Sp1 was associated as a heterocomplex with p53. Formation of this complex was dependent on the level of p53 since p53 was more abundant in proliferating cells and decreased upon induction of growth arrest and apoptosis by withdrawal of GM-CSF while Sp1 levels remained unchanged. These results suggest that the association of Sp1 with p53 may represent a novel mechanism of growth regulation in cytokine-dependent leukemia cells.

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Crossref · 10.1016/s0021-9258(18)53046-5

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  • p53 was first reported to bind to coactivators including TATA-box binding protein, NF-Y, and Sp1, and to interfere with their transactivator function.

    “In 1993, p53 was first reported to bind to coactivators, including the TATA-box binding protein,73, 74 the CCAAT-box binding factor (NF-Y)75 and specificity protein 1 (Sp1) that binds to GC-boxes,76 and to interfere with their transactivator function.”

    From Census and evaluation of p53 target genes (2017) · cites this paper as [76]

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Authors
Borellini, F., & Glazer, R. I.
Affiliations
Georgetown University Medical Center (US)
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1993-04
Volume
268
Issue
11
Pages
7923-7928
ISSN
0021-9258 (ISSN-L)
OpenAlex
W1547769073
Cited by
147
References
48
Citations by year
2025: 1 · 2022: 1 · 2018: 1 · 2017: 2 · 2016: 3 · 2014: 4 · 2013: 1 · 2012: 2
FWCI
4.98
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ca054231-03)
  • National Cancer Institute (CA54231)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords
Sp1, p53, heterocomplexes, DNA binding, GM-CSF, erythroleukemia, TF-1 cell line, cell proliferation, growth regulation, apoptosis, growth arrest, transcription factor binding sites
MeSH terms
Base Sequence, Cell Division, Cell Nucleus, Chromatin, DNA-Binding Proteins, DNA, Neoplasm, Leukemia, Erythroblastic, Acute, Humans, Microscopy, Electron, Molecular Sequence Data, Oligodeoxyribonucleotides, Tumor Cells, Cultured, Tumor Suppressor Protein p53, Granulocyte-Macrophage Colony-Stimulating Factor, Sp1 Transcription Factor, Apoptosis

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