Alteration of gene expression in the colon of colorectal cancer model rat by dietary sodium gluconate.

Abstract

Butyrate induces apoptosis of various cancer cell lines in a p53-independent manner and inhibits the proliferation of cancer cells. In a previous report, we reported a significant reduction in tumor incidence in rat colon as a result of dietary sodium gluconate (GNA). The stimulation of apoptosis through enhanced butyrate production in the large intestine was involved in the antitumorigenic effect of GNA. In the present study, a cDNA microarray analysis was performed to investigate the particular mechanism involved in the antitumorigenic effect of GNA. Some up-regulated genes suggested by microarray analysis were further evaluated using real-time PCR. A microarray revealed that GNA regulates the expression of retinoic acid receptor (RAR) and retinoid X receptor (RXR), and several genes known as the target of retinoids in cancer cells. In other words, the antitumorigenic effect of GNA may involve the regulation of the retinoid signaling pathway by butyrate in a retinoid-independent manner.

• Authors: Chiyoko Kameue, Takamitsu Tsukahara, Kazunari Ushida
• Journal: Bioscience, biotechnology, and biochemistry (Biosci Biotechnol Biochem) Vol. 70 Issue 3 Pg. 606-14 (Mar 2006) ISSN: 0916-8451 [Print] England
• PMID: 16556975 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Gluconates
• Proto-Oncogene Proteins c-bcl-2
• RNA, Messenger
• Rara protein, rat
• Receptors, Retinoic Acid
• Retinoic Acid Receptor alpha
• Retinoid X Receptor gamma
• gluconic acid

Topics

• Animals
• Body Weight (drug effects)
• Colon (drug effects, metabolism, pathology)
• Colorectal Neoplasms (genetics, prevention & control)
• Disease Models, Animal
• Eating
• Gene Expression Regulation, Neoplastic (drug effects, genetics)
• Gluconates (pharmacology)
• Male
• Oligonucleotide Array Sequence Analysis
• Proto-Oncogene Proteins c-bcl-2 (genetics)
• RNA, Messenger (genetics)
• Rats
• Receptors, Retinoic Acid (genetics)
• Retinoic Acid Receptor alpha
• Retinoid X Receptor gamma (genetics)