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FEBS Lett. 1993 Jul 12;326(1-3):45-50.

Regulation of c-myc expression by sodium butyrate in the colon carcinoma cell line Caco-2.

Author information

1
Département d'anatomie et de biologie cellulaire, Faculté de Médecine, Université de Sherbrooke, Québec, Canada.

Abstract

The human colon carcinoma cell line Caco-2 spontaneously undergoes enterocytic differentiation in culture. We used sodium butyrate to modify differentiation and growth properties of this cell line and considered c-myc expression as a potential target. Degradation of normal c-myc mRNAs with a half-life of 20 min is not coupled to translation in this cell line, as determined by cycloheximide treatment. We show that butyrate reduces c-myc mRNA levels after a 30 min delay. Butyrate does not affect c-myc expression at the level of transcriptional initiation or elongation, as determined by run-on analysis, but at a post-transcriptional level. Cycloheximide blocks butyrate-dependent reduction of c-myc mRNA levels. Cross-linking experiments show that a 34 kDa protein binds specifically to the c-myc AU-rich instability determinant found in the 3'-untranslated region (ARE). Binding of this protein to the ARE is not modulated by butyrate or cycloheximide. These experiments suggest that butyrate induces a factor involved in c-myc mRNA degradation that differs from the known ARE-associated proteins. Post-transcriptional modification of gene expression could be one of the major targets for this anti-proliferative agent.

PMID:
8325387
DOI:
10.1016/0014-5793(93)81758-r
[Indexed for MEDLINE]
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