| First Author | Singh Y | Year | 2014 |
| Journal | Br J Cancer | Volume | 111 |
| Issue | 1 | Pages | 132-8 |
| PubMed ID | 24874479 | Mgi Jnum | J:213270 |
| Mgi Id | MGI:5584034 | Doi | 10.1038/bjc.2014.275 |
| Citation | Singh Y, et al. (2014) Genetic ablation of beta-catenin inhibits the proliferative phenotype of mouse liver adenomas. Br J Cancer 111(1):132-8 |
| abstractText | BACKGROUND: Aberrant activation of Wnt/beta-catenin has been implicated in various cancer-related processes, for example, proliferation or tumour cell survival. However, the exact mechanism by which beta-catenin provides liver tumour cells with a selective advantage is still unclear. This study was aimed to analyse growth behaviour and survival of beta-catenin-driven mouse liver tumours after beta-catenin ablation. METHODS: Transgenic mice with a controllable hepatocyte-specific knockout of Ctnnb1 (encoding beta-catenin) were generated and liver tumours were induced by means of a N-nitrosodiethylamine/phenobarbital tumour initiation/promotion protocol, which leads to the outgrowth of hepatocellular tumours with activated beta-catenin. Cre recombinase was activated and the effects of the knockout in the tumours were studied. RESULTS: Activation of Cre recombinase led to the knockout of Ctnnb1 in a fraction of tumour cells, thus resulting in the formation of two different tumour cell subpopulations, with or without beta-catenin. Comparative analysis of the two subpopulations revealed that cell proliferation was significantly decreased in Ctnnb1-deleted hepatoma cells, compared with the corresponding non-deleted cell population, whereas no increased rate of apoptosis after knockout of Ctnnb1 was observed. CONCLUSIONS: beta-catenin-dependent signalling is an important regulator of hepatoma cell growth in mice, but not a crucial factor in the regulation of tumour survival. |
