Bile acid–microbiota cross-talk plays a critical role in gastrointestinal inflammation and carcinogenesis. Bile acids, produced in the liver and metabolized by gut bacteria, are essential for maintaining gut microbiota balance, lipid and carbohydrate metabolism, insulin sensitivity, and innate immunity. Recent research highlights the complex interactions between bile acids and the gut microbiota in the context of colorectal cancer (CRC) and hepatocellular carcinoma (HCC). Two major bile acid-sensing receptors, farnesoid X receptor (FXR) and G protein-coupled bile acid receptor (TGR5), are involved in these processes. The gut microbiota influences bile acid metabolism, which in turn affects cancer development. Strategies to target microbiota-dependent bile acid metabolism are being explored for cancer therapy. Bile acids are synthesized in the liver through two pathways, and their metabolism involves transport and reabsorption in the gut. The enterohepatic circulation of bile acids is crucial for maintaining bile acid homeostasis. Bile acids can activate various receptors, including FXR, PXR, CAR, VDR, and TGR5, which regulate gene expression and cellular responses. Dysregulation of bile acid signaling and microbiota composition is linked to gastrointestinal diseases, including cancer. Bile acids can promote inflammation and carcinogenesis by inducing DNA damage, activating NF-κB, and increasing reactive oxygen species (ROS). The gut microbiota also influences bile acid profiles, which can affect FXR activity and bile acid homeostasis. In CRC, bile acids such as DCA and LCA are associated with increased cancer risk. The gut microbiota can produce these bile acids, which contribute to inflammation and tumor promotion. Bile acid signaling through FXR and TGR5 is involved in regulating inflammation, immune responses, and cancer progression. In HCC, bile acid accumulation and dysbiosis of the gut microbiota are linked to liver inflammation and cancer development. Bile acid signaling pathways, including FXR and TGR5, are critical for maintaining intestinal barrier function and preventing cancer. The interplay between bile acids, the gut microbiota, and host signaling pathways is essential for understanding and managing gastrointestinal cancers. Targeting bile acid metabolism and microbiota composition offers potential therapeutic strategies for cancer prevention and treatment. The role of bile acids in cancer development is complex, involving multiple signaling pathways and interactions with the gut microbiota. Understanding these mechanisms is crucial for developing effective interventions to prevent and treat gastrointestinal cancers.Bile acid–microbiota cross-talk plays a critical role in gastrointestinal inflammation and carcinogenesis. Bile acids, produced in the liver and metabolized by gut bacteria, are essential for maintaining gut microbiota balance, lipid and carbohydrate metabolism, insulin sensitivity, and innate immunity. Recent research highlights the complex interactions between bile acids and the gut microbiota in the context of colorectal cancer (CRC) and hepatocellular carcinoma (HCC). Two major bile acid-sensing receptors, farnesoid X receptor (FXR) and G protein-coupled bile acid receptor (TGR5), are involved in these processes. The gut microbiota influences bile acid metabolism, which in turn affects cancer development. Strategies to target microbiota-dependent bile acid metabolism are being explored for cancer therapy. Bile acids are synthesized in the liver through two pathways, and their metabolism involves transport and reabsorption in the gut. The enterohepatic circulation of bile acids is crucial for maintaining bile acid homeostasis. Bile acids can activate various receptors, including FXR, PXR, CAR, VDR, and TGR5, which regulate gene expression and cellular responses. Dysregulation of bile acid signaling and microbiota composition is linked to gastrointestinal diseases, including cancer. Bile acids can promote inflammation and carcinogenesis by inducing DNA damage, activating NF-κB, and increasing reactive oxygen species (ROS). The gut microbiota also influences bile acid profiles, which can affect FXR activity and bile acid homeostasis. In CRC, bile acids such as DCA and LCA are associated with increased cancer risk. The gut microbiota can produce these bile acids, which contribute to inflammation and tumor promotion. Bile acid signaling through FXR and TGR5 is involved in regulating inflammation, immune responses, and cancer progression. In HCC, bile acid accumulation and dysbiosis of the gut microbiota are linked to liver inflammation and cancer development. Bile acid signaling pathways, including FXR and TGR5, are critical for maintaining intestinal barrier function and preventing cancer. The interplay between bile acids, the gut microbiota, and host signaling pathways is essential for understanding and managing gastrointestinal cancers. Targeting bile acid metabolism and microbiota composition offers potential therapeutic strategies for cancer prevention and treatment. The role of bile acids in cancer development is complex, involving multiple signaling pathways and interactions with the gut microbiota. Understanding these mechanisms is crucial for developing effective interventions to prevent and treat gastrointestinal cancers.