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Transcription interruption may be a common mechanism of c-myc regulation during HL-60 differentiation.

Publication ,  Journal Article
McCachren, SS; Salehi, Z; Weinberg, JB; Niedel, JE
Published in: Biochem Biophys Res Commun
February 29, 1988

Human promyelocytic leukemia cells (HL-60) differentiate along a monocytoid pathway in response to recombinant human tumor necrosis factor or recombinant human interferon gamma. Together, these agents act synergistically to induce phenotypic differentiation. Since reduced expression of mRNA for the proto-oncogene c-myc correlates with differentiation of HL-60 cells induced by other agents, we tested the abilities of tumor necrosis factor and interferon gamma to regulate expression of c-myc mRNA. Tumor necrosis factor rapidly and effectively reduced c-myc mRNA levels. In contrast, interferon gamma did not affect c-myc mRNA levels, nor did it show synergy with tumor necrosis factor in reducing c-myc. Transcription run-on studies confirmed that tumor necrosis factor caused interruption of c-myc transcription after exon 1. Phorbol diesters also caused interruption of transcription of c-myc. Thus, interruption of transcription may be a common mode of regulation of c-myc during induced differentiation of HL-60 cells.

Duke Scholars

Published In

Biochem Biophys Res Commun

DOI

ISSN

0006-291X

Publication Date

February 29, 1988

Volume

151

Issue

1

Start / End Page

574 / 582

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Tumor Cells, Cultured
  • Transcription, Genetic
  • Recombinant Proteins
  • RNA, Messenger
  • Proto-Oncogenes
  • Proto-Oncogene Proteins c-myc
  • Proto-Oncogene Proteins
  • Proto-Oncogene Mas
  • Phorbol Esters
 

Citation

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MLA
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McCachren, S. S., Salehi, Z., Weinberg, J. B., & Niedel, J. E. (1988). Transcription interruption may be a common mechanism of c-myc regulation during HL-60 differentiation. Biochem Biophys Res Commun, 151(1), 574–582. https://doi.org/10.1016/0006-291x(88)90633-x
McCachren, S. S., Z. Salehi, J. B. Weinberg, and J. E. Niedel. “Transcription interruption may be a common mechanism of c-myc regulation during HL-60 differentiation.Biochem Biophys Res Commun 151, no. 1 (February 29, 1988): 574–82. https://doi.org/10.1016/0006-291x(88)90633-x.
McCachren SS, Salehi Z, Weinberg JB, Niedel JE. Transcription interruption may be a common mechanism of c-myc regulation during HL-60 differentiation. Biochem Biophys Res Commun. 1988 Feb 29;151(1):574–82.
McCachren, S. S., et al. “Transcription interruption may be a common mechanism of c-myc regulation during HL-60 differentiation.Biochem Biophys Res Commun, vol. 151, no. 1, Feb. 1988, pp. 574–82. Pubmed, doi:10.1016/0006-291x(88)90633-x.
McCachren SS, Salehi Z, Weinberg JB, Niedel JE. Transcription interruption may be a common mechanism of c-myc regulation during HL-60 differentiation. Biochem Biophys Res Commun. 1988 Feb 29;151(1):574–582.
Journal cover image

Published In

Biochem Biophys Res Commun

DOI

ISSN

0006-291X

Publication Date

February 29, 1988

Volume

151

Issue

1

Start / End Page

574 / 582

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Tumor Cells, Cultured
  • Transcription, Genetic
  • Recombinant Proteins
  • RNA, Messenger
  • Proto-Oncogenes
  • Proto-Oncogene Proteins c-myc
  • Proto-Oncogene Proteins
  • Proto-Oncogene Mas
  • Phorbol Esters