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Purpose  Glutamine plays an important role in cell viability and growth of various tumors. For the fetal subtype of hepatoblastoma, growth inhibition through glutamine depletion was shown. We studied glutamine depletion in embryonal cell lines of hepatoblastoma carrying different mutations. Since asparagine synthetase was identified as a prognostic factor and potential therapeutic target in adult hepatocellular carcinoma, we investigated the expression of its gene  ASNS  and of the gene  GLUL,  encoding for glutamine synthetase, in hepatoblastoma specimens and cell lines and investigated the correlation with overall survival.    Methods  We correlated  GLUL  and  ASNS  expression with overall survival using publicly available microarray and clinical data. We examined  GLUL  and  ASNS  expression by RT-qPCR and by Western blot analysis in the embryonal cell lines Huh-6 and HepT1, and in five hepatoblastoma specimens. In the same cell lines, we investigated the effects of glutamine depletion. Hepatoblastoma biopsies were examined for histology and  CTNNB1  mutations.    Results  High  GLUL  expression was associated with a higher median survival time. Independent of mutations and histology, hepatoblastoma samples showed strong  GLUL  expression and glutamine synthesis. Glutamine depletion resulted in the inhibition of proliferation and of cell viability in both embryonal hepatoblastoma cell lines.  ASNS  expression did not correlate with overall survival.    Conclusion  Growth inhibition resulting from glutamine depletion, as described for the hepatoblastoma fetal subtype, is also detected in established embryonal hepatoblastoma cell lines carrying different mutations. At variance with adult hepatocellular carcinoma, in hepatoblastoma asparagine synthetase has no prognostic significance.

journal of cancer research and clinical oncology

Hepatoblastoma: glutamine depletion hinders cell viability in the embryonal subtype but high GLUL expression is associated with better overall survival