Abstract
The gut bacterial community is involved in the metabolism of bile acids and short-chain fatty acids (SCFAs). Bile acids are involved in the absorption of fat and the regulation of lipid homeostasis through emulsification and are transformed into unconjugated bile acids by the gut microbiota. The gut microbiota is actively involved in the production of bile acid metabolites, such as deoxycholic acid, lithocholic acid, choline, and SCFAs such as acetate, butyrate, and propionate. Metabolites derived from the gut microbiota or modified gut microbiota metabolites contribute significantly to host pathophysiology. Gut bacterial metabolites, such as deoxycholic acid, contribute to the development of hepatocellular carcinoma and colon cancer by factors such as inflammation and oxidative DNA damage. Butyrate, which is derived from gut bacteria such as Megasphaera, Roseburia, Faecalibacterium, and Clostridium, is associated with the activation of Treg cell differentiation in the intestine through histone acetylation. Butyrate averts the action of class I histone deacetylases (HDAC), such as HDAC1 and HDAC3, which are responsible for the transcription of genes such as p21/Cip1, and cyclin D3 through hyperacetylation of histones, which orchestrates G1 cell cycle arrest. It is essential to identify the interaction between the gut microbiota and bile acid and SCFA metabolism to understand their role in gastrointestinal carcinogenesis including colon, gastric, and liver cancer. Metagenomic approaches with bioinformatic analyses are used to identify the bacterial species in the metabolism of bile acids and SCFAs. This review provides an overview of the current knowledge of gut microbiota-derived bile acid metabolism in tumor development and whether it can stand as a marker for carcinogenesis. Additionally, this review assesses the evidence of gut microbiota-derived short-chain fatty acids including butyric acid in antitumor activity. Future research is required to identify the beneficial commensal gut bacteria and their metabolites which will be considered to be therapeutic targets in inflammation-mediated gastrointestinal cancers.
Highlights
Diet and endogenous synthetic pathways are the sources of lipids for normal cells [1]
We have discussed the crosstalk between gut microbiota and bile acid metabolism in the development of gastrointestinal cancers, such as CRC and hepatocellular carcinoma (HCC)
Short-chain fatty acids (SCFAs), such as acetate, butyrate, and propionate derived by gut microbiota, demonstrate inhibition of inflammation in gastrointestinal cancer through interaction with G protein-coupled receptors such as GPR41, GPR43, and GPR109A
Summary
Diet and endogenous synthetic pathways are the sources of lipids for normal cells [1]. Circulating lipids are involved in the synthesis of fatty acids, sphingolipids, phospholipids, cholesterol, and isoprenoids in normal cells [2]. Gut microbiota is involved in the production of secondary bile acids such as deoxycholic acid (DCA), lithocholic acid (LCA), choline, and short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate [4]. Gut bacterial metabolite DCA induces the development of gastrointestinal tumors such as hepatocellular carcinoma through inflammation [16] Bile acids such as DCA, LCA, chenodeoxycholic acid (CDCA), and taurochenodeoxycholic acid (TCDCA) demonstrate carcinogenic activity [17]. We mainly discuss the interaction between the dysbiosis of the gut microbiome and cholesterol/lipid metabolism in the development of cancer
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