Proteome analysis of chemically induced mouse liver tumors with different genotype

Julia Strathmann, Krisztina Paal, Carina Ittrich, Eberhard Krause, Klaus E. Appel, Howard P. Glauert, Albrecht Buchmann, Michael Schwarz

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


Mouse liver tumors frequently harbor mutations in Ha-ras, B-raf, or Ctnnb1 (encoding β-catenin). We conducted a proteome analysis with protein extracts from normal mouse liver and from liver tumors which were induced by a single injection of N-nitrosodiethylamine (DEN) as initiator followed by multiple injections of two different polychlorinated biphenyls (PCBs) as tumor promoters, or corn oil as a control. Liver tumors were stratified into two classes: they were either mutated in Ctnnb1 and positive for the marker glutamine synthetase (GS(+)), or they lacked Ctnnb1 mutations and were therefore GS-negative (GS(-)). Proteome analysis by 2-DE and MS revealed 98 significantly deregulated proteins, 44 in GS(+) and 54 in GS(-) tumors. Twelve of these proteins showed expression changes in both tumor types, but only seven of them were deregulated in the same direction. Several of the identified enzymes could be assigned to fundamental metabolic or other cellular pathways with characteristically different alterations in GS(+) and GS(-) tumors such as ammonia and amino acid turnover, cellular energy supply, and calcium homeostasis. Our data suggest that GS(+) and GS(-) tumor cells show a completely different biology and use divergent evolutionary strategies to gain a selective advantage over normal hepatocytes.

Original languageEnglish
Pages (from-to)3318-3331
Number of pages14
Issue number18
StatePublished - Sep 2007


  • Ha-ras
  • Hepatocarcinogenesis
  • Liver tumors
  • β-Catenin

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology


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