Proteome Differences between Hepatitis B Virus Genotype-B- and Genotype-C-Induced Hepatocellular Carcinoma Revealed by iTRAQ-Based Quantitative Proteomics

J Proteome Res. 2016 Feb 5;15(2):487-98. doi: 10.1021/acs.jproteome.5b00838. Epub 2016 Jan 14.

Abstract

Hepatitis B virus (HBV) is the main cause of hepatocellular carcinoma (HCC) in southeast Asia where HBV genotype B and genotype C are the most prevalent. Viral genotypes have been reported to significantly affect the clinical outcomes of HCC. However, the underlying molecular differences among different genotypes of HBV virus infected HCC have not been revealed. Here, we applied isobaric tags for relative and absolute quantitation (iTRAQ) technology integrated with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis to identify the proteome differences between the HBV genotypes B- and C-induced HCC. In brief, a total of 83 proteins in the surrounding noncancerous tissues and 136 proteins in the cancerous tissues between HBV genotype-B- and genotype-C-induced HCC were identified, respectively. This information revealed that there might be different molecular mechanisms of the tumorigenesis and development of HBV genotypes B- and C-induced HCC. Furthermore, our results indicate that the two proteins ARFIP2 and ANXA1 might be potential biomarkers for distinguishing the HBV genotypes B- and C-induced HCC. Thus, the quantitative proteomic analysis revealed molecular differences between the HBV genotypes B- and C-induced HCC, and might provide fundamental information for further deep study.

Keywords: ANXA1; ARFIP2; HBV genotype B and genotype C; hepatocellular carcinoma; quantitative proteomics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / virology
  • Chromatography, Liquid
  • Female
  • Gene Expression Regulation, Neoplastic
  • Gene Ontology
  • Genotype
  • Hepatitis B / genetics
  • Hepatitis B / metabolism*
  • Hepatitis B / virology
  • Hepatitis B virus / genetics
  • Hepatitis B virus / physiology
  • Host-Pathogen Interactions
  • Humans
  • Isotope Labeling / methods
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / virology
  • Male
  • Middle Aged
  • Proteome / genetics
  • Proteome / metabolism*
  • Proteomics / methods*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tandem Mass Spectrometry

Substances

  • Biomarkers, Tumor
  • Proteome