Regulation of c-myc RNA and its proteins in Daudi cells by interferon-beta.

Abstract

It has been shown previously that interferons (IFNs) -alpha and -beta cause a reduction in the steady-state level of poly(A) c-myc RNA in the Burkitt lymphoma, Daudi. In this report we show that the c-myc RNA reduction is not mediated by simple changes in the poly-adenylation of either nascent or existing c-myc transcripts, since similar reductions of c-myc sequences were observed in poly(A) and total cellular RNA preparations from IFN-beta-treated cells. Furthermore, the first exon of c-myc RNA in Daudi cells contains several mutations, suggesting that the germ line configuration of the first exon is not essential for the IFN-beta-mediated regulation. The c-myc RNA reduction was also detected in cells whose protein synthesis was inhibited by more than 95% with cycloheximide or emetine. We surmise that neither sustained nor IFN-induced protein synthesis is required for the c-myc RNA regulation. Antisera raised against either the carboxy- or amino-terminal c-myc peptides precipitate in Daudi cells proteins of 66,000 and 63,000 daltons. In cells treated with IFN-beta, the amounts of these proteins are reduced by 46-74% which is in agreement with the reduction detected at the level of c-myc RNA.

• Authors: G J Jonak, B K Friedland, E D Anton, E Knight Jr
• Journal: Journal of interferon research (J Interferon Res) Vol. 7 Issue 1 Pg. 41-52 (Feb 1987) ISSN: 0197-8357 [Print] United States
• PMID: 3295065 (Publication Type: Journal Article)

Chemical References

• Interferon Type I
• Proto-Oncogene Proteins
• RNA, Neoplasm
• Cycloheximide

Topics

• Burkitt Lymphoma (genetics, metabolism, therapy)
• Cell Line
• Cycloheximide (pharmacology)
• Exons
• Gene Expression Regulation (drug effects)
• Humans
• Interferon Type I (pharmacology)
• Proto-Oncogene Proteins (genetics, metabolism)
• Proto-Oncogenes
• RNA, Neoplasm (genetics, metabolism)