Differential effects of inactivated Axin1 and activated beta-catenin mutations in human hepatocellular carcinomas.
作者： J Zucman-Rossi , S Benhamouche , C Godard , S Boyault , G Grimber
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摘要: Perturbations to the Wnt signaling pathway have been implicated in a large proportion of human hepatocellular carcinomas (HCCs). Activating β-catenin mutations and loss function Axin1 are thought be functionally equivalent. We examined HCC by comparing expression target genes level β-catenin-dependent transcriptional activation, 45 tumors four cell lines. Among these samples, AXIN1 were mutated 20 seven cases, respectively. found significant correlation between activated overexpression mRNA for glutamine synthetase (GS), G-protein-coupled receptor (GPR)49 glutamate transporter (GLT)-1 (P=0.0001), but not ornithine aminotransferase, LECT2, c-myc cyclin D1. also showed that GS is good immunohistochemical marker activation HCC. However, we observed no induction GS, GPR49 or GLT-1 five inactivated tumors. β-Catenin-dependent two Axin1-mutated lines was much weaker than β-catenin-mutated Our results strongly suggest HCC, contrary expectation, equivalent gain β-catenin. tumor suppressor may related another, non-Wnt pathway.
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