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"Liver-on-a-Chip" Cultures of Primary Hepatocytes and Kupffer Cells for Hepatitis B Virus Infection
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Multi-omics analyses reveal metabolic alterations regulated by hepatitis B virus core protein in hepatocellular

Qi Xie1,2, Fengxu Fan2,3, Wei Wei2

  • 1School of Basic Medical Sciences, Key Laboratory of Combinatorial Biosynthesis and Drug Discovery of Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan 430071, China.

Scientific Reports
|January 24, 2017
PubMed

Insights

Hepatitis B virus core protein (HBc) promotes liver cancer by altering cell metabolism. HBc enhances glycolysis and amino acid metabolism in hepatocellular carcinoma cells, suggesting a key role in disease development.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Cancer Research

Background:

  • Chronic hepatitis B virus (HBV) infection is linked to liver diseases, including hepatocellular carcinoma (HCC).
  • The precise role of HBV core protein (HBc) in the pathogenesis of liver disease remains incompletely understood.
  • Investigating HBc's function is crucial for understanding HBV-related liver disease progression.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which HBc influences hepatocellular carcinoma (HCC) cells.
  • To explore the impact of HBc on cellular metabolism in the context of liver cancer.
  • To identify potential regulatory pathways involving HBc in HCC development.

Main Methods:

  • Multi-omics analyses, including proteomics and metabolomics, were employed.
  • Hepatocellular carcinoma (HCC) cells transfected with HBc were utilized for characterization.
  • Analysis focused on changes in protein expression, metabolite secretion, and key metabolic pathways.

Main Results:

  • HBc significantly promoted the expression of metabolic enzymes and the secretion of metabolites in HCC cells.
  • Glycolysis and amino acid metabolism were found to be significantly up-regulated by HBc.
  • Evidence suggests HBc recruits Max-like protein X (MLX) to the nucleus, potentially regulating glycolysis.

Conclusions:

  • Metabolic reprogramming is a key hallmark of HBc transfection in HCC cells.
  • HBc plays a significant role in altering cellular metabolism, contributing to the molecular pathogenesis of HBV-induced liver diseases.
  • These findings offer new insights into HBc's function and potential therapeutic targets in HBV-related HCC.

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