Abstract
Introduction: SLC5A8, expressed predominantly in the colon, is a Na +-coupled transporter for short-chain fatty acids. In this paper, we report on the characterization of butyrate transport by SLC5A8 and the relevance of SLC5A8-mediated butyrate transport to colon cancer. Results: SLC5A8 transports butyrate via a Na+-dependent electrogenic process. Na + activation of the transport process exhibits sigmoidal kinetics, indicating involvement of more than one Na+ in the activation process. SLC5A8 is silenced in colon cancer in humans, in a mouse model of intestinal/colon cancer, and in colon cancer cell lines. The tumor-associated silencing of SLC5A8 involves DNA methylation by DNA methyltransferase 1. Reexpression of SLC5A8 in colon cancer cells leads to apoptosis but only in the presence of butyrate. SLC5A8-mediated entry of butyrate into cancer cells is associated with inhibition of histone deacetylation. The changes in gene expression in SLC5A8/butyrate-induced apoptosis include upregulation of pro-apoptotic genes and downregulation of anti-apoptotic genes. In addition, the expression of phosphatidylinositol-3-kinase subunits is affected differentially, with downregulation of p85α and upregulation of p55α and p50α. Conclusion: These studies show that SLC5A8 mediates the tumor-suppressive effects of the bacterial fermentation product butyrate in the colon.
Original language | English (US) |
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Pages (from-to) | 1773-1781 |
Number of pages | 9 |
Journal | Journal of Gastrointestinal Surgery |
Volume | 12 |
Issue number | 10 |
DOIs | |
State | Published - Oct 1 2008 |
Keywords
- Colon cancer
- Commensal bacteria
- DNA methylation
- Dietary fiber
- Histone deacetylation
- Tumor suppression
ASJC Scopus subject areas
- Surgery
- Gastroenterology