Regulation of c-myc RNA and its proteins in Daudi cells by interferon-beta.
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.
Jonak
G J
GJ
Friedland
B K
BK
Anton
E D
ED
Knight
E
E
D002051:Burkitt Lymphoma / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D005091:Exons; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007370:Interferon Type I / Q000494:pharmacology*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D011519:Proto-Oncogenes; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism*
D007370:Interferon Type I; D011518:Proto-Oncogene Proteins; D012334:RNA, Neoplasm; D003513:Cycloheximide