Journal
NATURE CANCER
Volume 2, Issue 10, Pages 1039-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/s43018-021-00251-3
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Funding
- US National Institutes of Health [AI072360]
- JSPS KAKENHI [JP25893081]
- Harvard-wide Program on Antibiotic Resistance [AI083214]
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The study revealed that Enterococcus faecalis is abundant in the microbiota of patients with hepatitis C virus-related chronic liver disease, promoting liver carcinogenesis via the TLR4-Myd88 signaling pathway.
Mizukoshi and colleagues use patient samples and xenotransplants to show that the microbiota associated with chronic liver disease promote liver carcinogenesis through gelE-positive Enterococcus faecalis via induction of TLR4-Myd88 signaling. Gut dysbiosis is observed in chronic hepatobiliary diseases and is frequently associated with liver carcinogenesis; however, the extent and specific mechanisms triggered by alterations in the microbiota mediating tumorigenesis in these patients remain unclear. Here we show that Enterococcus faecalis is abundant in the microbiota of patients with hepatitis C virus-related chronic liver disease. Xenotransplantation of gut microbiota from these patients increased the number of spontaneous liver tumors in mice and enhanced susceptibility to liver carcinogens. Hepatic colonization by gelE-positive E. faecalis increased liver expression of proliferative genes in a TLR4-Myd88-dependent manner, leading to liver tumorigenesis. Moreover, decreased fecal deoxycholic acid levels were associated with colonization by E. faecalis. Overall, these data identify E. faecalis as a key promoter of liver carcinogenesis.
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