Transcriptional activation of the translocated c-myc oncogene in mouse plasmacytomas: Similar RNA levels in tumor and proliferating normal cells

Elizabeth J. Keath, Ameeta Kelekar, Michael D. Cole

Research output: Contribution to journalArticlepeer-review

53 Scopus citations

Abstract

We examine the influence of the immunoglobulin locus on the expression of the translocated c-myc oncogene in mouse plasmacytomas. The level of c-myc RNA was 30- 35-fold greater in tumor cells than in normal, quiescent B cells. Mitogen stimulation of the lymphocytes with lipopolysaccharide induced a 15-fold increase in c-myc expression per cell to a level that was similar to that in the tumor cells. Northern blot analysis showed that transcription of the translocated c-myc gene involved initiation from sequences in the first c-myc intron. Abundant RNA transcripts were also found from the noncoding strand of the c-myc intron in most tumor lines. S1 nuclease mapping was used to locate the intronic sequences that are used to initiate the tumor-specific c-myc RNAs. Six different initiation sites within the intron were mapped, none of which have the TATA sequence usually associated with eucaryotic RNA polymerase II promoters. The noncoding strand transcripts were also found to initiate in the c-myc intron. Transcription of the c-myc coding strand was independent of the position of the translocation breakpoint, even when the heavy chain switch and constant regions were deleted.

Original languageEnglish (US)
Pages (from-to)521-528
Number of pages8
JournalCell
Volume37
Issue number2
DOIs
StatePublished - Jun 1984

Bibliographical note

Funding Information:
We would like to thank Jim Battey and Donal Luse for helpful discussions. This work was supported by grants from the National Cancer Institute and the Sklarow Memorial Trust.

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