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Regulation of c‐ myc expression by sodium butyrate in the colon carcinoma cell line Caco‐2
Author(s) -
Souleimani Abdellah,
Asselin Claude
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)81758-r
Subject(s) - sodium butyrate , cycloheximide , butyrate , cell culture , messenger rna , caco 2 , microbiology and biotechnology , translation (biology) , gene expression , biology , untranslated region , protein biosynthesis , cell , chemistry , gene , biochemistry , genetics , fermentation
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.