Expression of normal and translocated c-myc alleles in Burkitt's lymphoma cells: evidence for different regulation.

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Abstract
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.