1. Figure 1 Contribution of the gut microbiota
to hepatocarcinogenesis: mechanisms and therapeutic targets
Figure 1 | Contribution of the gut microbiota to hepatocarcinogenesis: mechanisms and therapeutic targets. Dysbiosis and the leaky gut promote the progression of liver disease and the development of hepatocellular carcinoma (HCC) via multiple mechanisms, including the release of cancer-promoting and senescence-promoting metabolites such as deoxycholic acid (DCA) from the dysbiotic microbiota, and increased hepatic exposure to gut-derived microbiota-associated molecular patterns (MAMPs) such as lipopolysaccharide (LPS), which in turn promote hepatic inflammation, fibrosis, proliferation and the activation of anti-apoptotic signals. These cancer-promoting signalling pathways can be interrupted at several levels: using probiotics to restore eubiosis; using antibiotics to eliminate disease-promoting bacteria and decrease the release of MAMPs and metabolites from the leaky gut; using agents to improve the gut barrier; and potentially using inhibitors of bacterial metabolism to reduce the production of cancer-promoting metabolites by the gut microbiota. FXR, farnesoid X receptor; HSC, hepatic stellate cell; TLR, Toll-like receptor; SASP, senescence-associated secretory phenotype.
Yu, L.-X. & Schwabe, R. F. (2017) The gut microbiome and liver cancer: mechanisms and clinical translation
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro