Alteration of Gene Expression in the Colon of Colorectal Cancer Model Rat by Dietary Sodium Gluconate | Zendy

Chiyoko Kameue | Zendy; Takamitsu Tsukahara | Zendy; Kazunari Ushida | Zendy

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Alteration of Gene Expression in the Colon of Colorectal Cancer Model Rat by Dietary Sodium Gluconate

Author(s) -

Chiyoko Kameue,

Takamitsu Tsukahara,

Kazunari Ushida

Publication year - 2006

Publication title -

bioscience biotechnology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.509

H-Index - 116

eISSN - 1347-6947

pISSN - 0916-8451

DOI - 10.1271/bbb.70.606

Subject(s) - retinoid , retinoid x receptor , sodium butyrate , butyrate , microarray analysis techniques , biology , microarray , retinoic acid , colorectal cancer , cancer research , apoptosis , gene expression , gene chip analysis , cancer , gene , microbiology and biotechnology , biochemistry , genetics , transcription factor , nuclear receptor , fermentation

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.

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