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Free fatty acid receptor 2 ( FFAR2 ) has been reported as a tumor suppressor in colon cancer development. The current study investigated the effects of FFAR2 signaling on energy metabolism and gut microbiota profiling in a colorectal cancer mouse model ( Apc   Min/+  ). Ffar2 deficiency promoted colonic polyp development and enhanced fatty acid oxidation and bile acid metabolism. Gut microbiome sequencing analysis showed distinct clustering among wild-type, Apc   Min/+  , and Apc   Min/+  - Ffar2  -/- mice. The relative abundance of Flavobacteriaceae and Verrucomicrobiaceae was significantly increased in the Apc   Min/+  - Ffar2  -/- mice compared to the Apc   Min/+  mice. In addition, knocking-down FFAR2 in the human colon cancer cell lines (SW480 and HT29) resulted in increased expression of several key enzymes in fatty acid oxidation, such as carnitine palmitoyltransferase 2, acyl-CoA dehydrogenase, long-chain acyl-CoA dehydrogenase, C-2 to C-3 short chain, and hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase, alpha subunit. Collectively, these results demonstrated that Ffar2 deficiency significantly altered profiles of fatty acid metabolites and gut microbiome, which might promote colorectal cancer development.

journal of cancer prevention

Dysregulated Free Fatty Acid Receptor 2 Exacerbates Colonic Adenoma Formation in <i>Apc<sup>Min/+</sup></i> Mice: Relation to Metabolism and Gut Microbiota Composition

Dysregulated Free Fatty Acid Receptor 2 Exacerbates Colonic Adenoma Formation in ApcMin/+ Mice: Relation to Metabolism and Gut Microbiota Composition

Dysregulated Free Fatty Acid Receptor 2 Exacerbates Colonic Adenoma Formation in Apc^Min/+ Mice: Relation to Metabolism and Gut Microbiota Composition