Gene expression profiles of Caco-2 cells treated with cholic acid

Colorectal cancer (CRC) is the third most common cancer in men and the second in women worldwide, with most of the case occurrences in developed regions. CRC can be induced by luminal factors, like dietary components and bile acids. Bile acids are metabolized from cholesterol in the liver, stored in the gallbladder and released into the small intestine upon meal ingestion to facilitate the absorption of dietary lipids and lipid-soluble vitamins. Bile acids are effectively reabsorbed at the distal ileum and returned to the liver, and only a small portion (~2-5%) enters the colon. Here primary bile acids, like cholic acid (CA) and chenodeoxycholic acid (CDCA) are deconjugated by bacteria and secondary bile acids are formed, such as deoxycholic acid (DCA), ursodeoxycholic acid (UDCA) and lithocholic acid. DCA is the major component of the colonic bile acid pool and is found to be increased upon a high fat diet. Moreover, high levels of DCA are known to increase the risk of colorectal cancer by inducing cytotoxicity to epithelial cells. In this study the cytotoxicity of Caco-2 cells to stimulation with cholic acid is investigated. Caco-2 cells were cultured on collagen-coated transwell or regular cell culture plates and incubated in the presence or absence of the bile acid cholate. Pooled RNA samples were subjected to expression profiling.