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Eick, D. ; Bornkamm, G.W.

Expression of Normal and Translocated c-myc Alleles in Burkitt's Lymphoma Cells: Evidence for Different Regulation.

EMBO J. 8, 1965-1972 (1989)
DOI PMC
Open Access Gold möglich sobald Verlagsversion bei der ZB eingereicht worden ist.
In Burkitt's lymphoma (BL) cells the normal c-myc allele is usually silent or expressed at very low levels. Here we demonstrate that the normal c-myc allele can be induced in BL cells by 12-O-tetradecanoylphorbol-13-acetate (TPA). TPA did activate the normal c-myc alleles in Raji(P207), BL36, P3HR1, Jijoye and LY91 cells, but not in Raji(DE88), BL41, BL67, LY47 and KK124 cells. C-myc RNA derived from the normal allele appeared 6 h after treatment with TPA and showed the characteristic preferential usage of the second promoter. This induction could not be inhibited by cycloheximide. Despite the differences in c-myc induction in Raji(P207) and Raji(DE88) cells, c-fos and the early Epstein-Barr virus gene DR were induced to a similar extent and with similar kinetics by TPA. Nuclear run-on experiments suggest that the normal c-myc allele in Raji cells is activated at least in part by releasing a block to RNA elongation at the end of c-myc exon 1. Expression of the translocated c-myc alleles was also affected by TPA; however, only if cycloheximide was simultaneously present. TPA plus cycloheximide induced a rapid decrease of c-myc RNA derived from the translocated allele within 6 h, whereas cycloheximide alone led to abolition of c-myc RNA after 16-24 h. This rapid decline of c-myc RNA was observed in Raji and BL41 cells, but not in three cell lines with variant t(2;8) and t(8;22) translocations.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 0261-4189
e-ISSN 1460-2075
Zeitschrift EMBO Journal, The
Quellenangaben Band: 8, Heft: 7, Seiten: 1965-1972 Artikelnummer: , Supplement: ,
Verlag Wiley
Verlagsort Heidelberg, Germany
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)