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Truncation Does Not Abrogate Transcriptional Downregulation of the C-myc Gene by Sodium Butyrate in Burkitt's Lymphoma Cells

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Journal EMBO J
Date 1987 Oct 1
PMID 3691477
Citations 13
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Abstract

We have examined the effect of sodium butyrate, a potent inducer of differentiation in various cell systems, on the steady state RNA level and transcriptional activity of the c-myc gene in Burkitt's lymphoma cells. Following sodium butyrate treatment a rapid decrease of c-myc RNA was observed in all Burkitt's lymphoma cell lines studied, irrespective of the type of translocation, the location of the breakpoint relative to c-myc or of the association with EBV. Since cellular genes induced by interferon are suspected to play a role in c-myc regulation we have studied transcription of the 2-5A synthetase gene in sodium butyrate-treated Burkitt's lymphoma cells. Transcriptional activity and steady state mRNA levels of the 2-5A synthetase gene were induced by sodium butyrate. The time course of induction excluded, however, that the decrease of c-myc RNA is caused by induction of the 2-5A synthetase/RNase L endonuclease system. The reduction of c-myc RNA is caused, at least in part, by a reduced transcription rate, as shown by nuclear run-on analysis. The fact that sodium butyrate is capable of downregulating a truncated c-myc gene indicates that an important target site of transcriptional regulation is located outside the region encompassing the upstream regulatory sequences, the dual promoters and the leader region.

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References
1.
Leder A, Leder P . Butyric acid, a potent inducer of erythroid differentiation in cultured erythroleukemic cells. Cell. 1975; 5(3):319-22. DOI: 10.1016/0092-8674(75)90107-5. View

2.
Southern E . Detection of specific sequences among DNA fragments separated by gel electrophoresis. J Mol Biol. 1975; 98(3):503-17. DOI: 10.1016/s0022-2836(75)80083-0. View

3.
Collins S, Ruscetti F, Gallagher R, Gallo R . Terminal differentiation of human promyelocytic leukemia cells induced by dimethyl sulfoxide and other polar compounds. Proc Natl Acad Sci U S A. 1978; 75(5):2458-62. PMC: 392573. DOI: 10.1073/pnas.75.5.2458. View

4.
Andersson L, Jokinen M, Gahmberg C . Induction of erythroid differentiation in the human leukaemia cell line K562. Nature. 1979; 278(5702):364-5. DOI: 10.1038/278364a0. View

5.
Luka J, Kallin B, Klein G . Induction of the Epstein-Barr virus (EBV) cycle in latently infected cells by n-butyrate. Virology. 1979; 94(1):228-31. DOI: 10.1016/0042-6822(79)90455-0. View