Sodium Butyrate Increases Expression of the Coxsackie and Adenovirus Receptor in Colon Cancer Cells

ABSTRACT Histone deacetylase inhibitors (HDACI), e.g., sodium butyrate (NaB), have been suggested to upregulate the coxsackie and adenovirus receptor (CAR). Its impact on CAR in colon carcinomas, however, is poorly understood. NaB treatment of colon cancer cells increased CAR expression preferential...

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Bibliographic Details
Published in:Cancer investigation 2010-03, Vol.28 (3), p.268-274
Main Authors: Küster, Katrin, Grötzinger, Carsten, Koschel, Annika, Fischer, Andreas, Wiedenmann, Bertram, Anders, Mario
Format: Article
Language:English
Subjects:
Animals
Butyrates - pharmacology
Caco-2 Cells
Cell Differentiation
CHO Cells
Colon cancer
Colonic Neoplasms - drug therapy
Colonic Neoplasms - metabolism
Colonic Neoplasms - pathology
Coxsackie adenovirus receptor
Coxsackie and Adenovirus Receptor-Like Membrane Protein
Cricetinae
Cricetulus
Differentiation
Histone deacetylase inhibition
Histone Deacetylase Inhibitors - pharmacology
Histone Deacetylase Inhibitors - therapeutic use
Humans
Receptors, Virus - drug effects
Receptors, Virus - genetics
RNA, Messenger - analysis
Sodium butyrate
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Summary:ABSTRACT Histone deacetylase inhibitors (HDACI), e.g., sodium butyrate (NaB), have been suggested to upregulate the coxsackie and adenovirus receptor (CAR). Its impact on CAR in colon carcinomas, however, is poorly understood. NaB treatment of colon cancer cells increased CAR expression preferentially in cell lines with low basic CAR levels. These findings suggest that downregulation of CAR gene expression is mediated by transcriptional regulation and that activation of the CAR gene promoter is modulated by histone acetylation. The employment of HDACI may, therefore, represent a promising approach for improving adenovirus-based therapies of colon cancers with low CAR expression levels.
ISSN:0735-7907
1532-4192
DOI:10.3109/07357900902783195