Gut microbial dysbiosis associates hepatocellular carcinoma via the gut-liver axis

Hepatobiliary Pancreat Dis Int. 2019 Feb;18(1):19-27. doi: 10.1016/j.hbpd.2018.11.002. Epub 2018 Nov 22.

Abstract

Background: Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world. Gut microbiota has been demonstrated to play a critical role in liver inflammation, chronic fibrosis, liver cirrhosis, and HCC development through the gut-liver axis.

Data sources: Recently there have been several innovative studies investigating gut microbial dysbiosis-mediated enhancement of HCC through the gut-liver axis. Literatures from January 1998 to January 2018 were searched in the PubMed database using the keywords "gut microbiota" and "hepatocellular carcinoma" or "liver cancer", and the results of experimental and clinical studies were analyzed.

Results: Gut microbial dysbiosis accompanies the progression of alcoholic liver disease, non-alcoholic fatty liver disease and liver cirrhosis, and promotes HCC progression in an experimental mouse model. The immune system and key factors such as Toll-like receptor 4 are involved in the process. There is evidence for gut microbial dysbiosis in hepatitis virus-related HCC patients.

Conclusions: Gut microbial dysbiosis is closely associated with hepatic inflammation disease and HCC through the gut-liver axis. With the enhanced understanding of the interactions between gut microbiota and liver through the gut-liver axis, new treatment strategies for HCC are being developed.

Keywords: Gut microbiota; Gut-liver axis; Hepatocellular carcinoma; Lipopolysaccharide; Toll-like receptor 4.

Publication types

  • Review

MeSH terms

  • Animals
  • Carcinoma, Hepatocellular / metabolism
  • Carcinoma, Hepatocellular / microbiology*
  • Carcinoma, Hepatocellular / pathology
  • Carcinoma, Hepatocellular / virology
  • Cell Transformation, Neoplastic / metabolism
  • Cell Transformation, Neoplastic / pathology
  • Dysbiosis*
  • Gastrointestinal Microbiome*
  • Hepatitis B / microbiology
  • Hepatitis B / virology
  • Host-Pathogen Interactions
  • Humans
  • Liver / metabolism
  • Liver / microbiology*
  • Liver / pathology
  • Liver / virology
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / microbiology*
  • Liver Neoplasms / pathology
  • Liver Neoplasms / virology
  • Prognosis
  • Risk Factors
  • Signal Transduction
  • Toll-Like Receptor 4 / metabolism

Substances

  • Toll-Like Receptor 4