Selective inhibition of c-myc expression by the ribonucleic acid synthesis inhibitor mithramycin

Vicki V. Baker, Hugh M. Shingleton, Kenneth D Hatch, Donald M. Miller

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Expression of the c-myc proto-oncogene has been shown to correlate with the rate of cellular proliferation and malignant transformation in a number of cell types. JEG-3 choriocarcinoma cells demonstrate c-myc transcript levels that are greater than those of nonmalignant trophoblastic tissue at any stage of gestation. Southern blot analysis documents c-myc gene amplification in JEG 3 cells, with a gene copy number of approximately 20. The methylation pattern and genomic structure of the amplified c-myc oncogene in JEG-3 choriocaricoma cells are identical to those of normal placenta. Treatment of JEG-3 cells with mithramycin, a ribonucleic acid synthesis inhibitor, results in a dramatic decrease in c-myc expression relative to that of the c-Ha-Ras gene. The apparent selectivity of mithramycin for c-myc expression represents the only example, to date, of the selective pharmacologic modulation of oncogene expression.

Original languageEnglish (US)
Pages (from-to)762-767
Number of pages6
JournalAmerican Journal of Obstetrics and Gynecology
Volume158
Issue number4
DOIs
StatePublished - 1988
Externally publishedYes

Fingerprint

Plicamycin
myc Genes
RNA
Choriocarcinoma
Gene Dosage
ras Genes
Gene Amplification
Southern Blotting
Oncogenes
Placenta
Methylation
Cell Count
Cell Proliferation
Pregnancy

Keywords

  • c-myc proto-oncogene
  • choriocarcinoma cells in culture
  • inhibition by mithramycin

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Selective inhibition of c-myc expression by the ribonucleic acid synthesis inhibitor mithramycin. / Baker, Vicki V.; Shingleton, Hugh M.; Hatch, Kenneth D; Miller, Donald M.

In: American Journal of Obstetrics and Gynecology, Vol. 158, No. 4, 1988, p. 762-767.

Research output: Contribution to journalArticle

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AB - Expression of the c-myc proto-oncogene has been shown to correlate with the rate of cellular proliferation and malignant transformation in a number of cell types. JEG-3 choriocarcinoma cells demonstrate c-myc transcript levels that are greater than those of nonmalignant trophoblastic tissue at any stage of gestation. Southern blot analysis documents c-myc gene amplification in JEG 3 cells, with a gene copy number of approximately 20. The methylation pattern and genomic structure of the amplified c-myc oncogene in JEG-3 choriocaricoma cells are identical to those of normal placenta. Treatment of JEG-3 cells with mithramycin, a ribonucleic acid synthesis inhibitor, results in a dramatic decrease in c-myc expression relative to that of the c-Ha-Ras gene. The apparent selectivity of mithramycin for c-myc expression represents the only example, to date, of the selective pharmacologic modulation of oncogene expression.

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