c-Myc-mediated expression of nucleophosmin/B23 decreases during retinoic acid-induced differentiation of human leukemia HL-60 cells

The retinoic acid-induced differentiation of human leukemia HL-60 cells towards mature granulocytic cells was accompanied by the decline in the protein levels of c-myc, nucleophosmin/B23 and its promoter activity. These RA-induced effects were further enhanced by the concurrent treatment of HL-60 ce...

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Bibliographic Details
Published inFEBS letters Vol. 578; no. 3; pp. 211 - 216
Main Author Yung, Benjamin Y.M.
Format Journal Article
LanguageEnglish
Published England Elsevier B.V 17.12.2004
Subjects
Antibodies, Monoclonal - metabolism
Blotting, Western
c-Myc
Cell Differentiation - drug effects
Chromatin Immunoprecipitation
Differentiation
Down-Regulation - drug effects
Enzyme Inhibitors - pharmacology
Fluorescein-5-isothiocyanate
Fluorescent Dyes
Gene Expression Regulation, Neoplastic - drug effects
HL-60 Cells
Humans
Imidazoles - pharmacology
Nuclear Proteins - metabolism
Nucleophosmin/B23
Oligonucleotides, Antisense - pharmacology
p38 Mitogen-Activated Protein Kinases - drug effects
Phosphoproteins - metabolism
Promoter Regions, Genetic
Proto-Oncogene Proteins c-myc - metabolism
Pyridines - pharmacology
Retinoic acid
Temperature
Time Factors
Transcription, Genetic - drug effects
Transcriptional regulation
Tretinoin - pharmacology
Transcriptional regulation
Differentiation
c-Myc
Retinoic acid
Nucleophosmin/B23
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Summary:The retinoic acid-induced differentiation of human leukemia HL-60 cells towards mature granulocytic cells was accompanied by the decline in the protein levels of c-myc, nucleophosmin/B23 and its promoter activity. These RA-induced effects were further enhanced by the concurrent treatment of HL-60 cells with p38 map kinase inhibitor SB203580 (SB). It seems that there is a strong correlation of nucleophosmin/B23 and c-Myc expressions in cells under RA treatment. Furthermore, nucleophosmin/B23 promoter activity decreased upon c-Myc antisense-mediated reduction of intracellular amount of c-Myc. CHIP assays showed that binding of c-Myc to the nucleophosmin/B23 promoter decreased in RA-treated cells. Thus, nucleophosmin/B23 expression is targeted by c-Myc during RA-induced differentiation. These results provide evidence for a novel mechanism of transcriptional downregulation of nucleophosmin/B23 and the functional role of c-Myc in RA-induced differentiation.
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ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2004.08.089