Cagatay, T.Ozturk, M.2016-02-082016-02-0820020950-9232http://hdl.handle.net/11693/24623β-catenin is involved in both cell-cell interactions and wnt pathway-dependent cell fate determination through its interactions with E-cadherin and TCF/LEF transcription factors, respectively. Cytoplasmic/nuclear levels of β-catenin are important in regulated transcriptional activation of TCF/LEF target genes. Normally, these levels are kept low by proteosomal degradation of β-catenin through Axin1- and APC-dependent phosphorylation by CKI and GSK-3β. Deregulation of β-catenin degradation results in its aberrant accumulation, often leading to cancer. Accordingly, aberrant accumulation of β-catenin is observed at high frequency in many cancers. This accumulation correlates with either mutational activation of CTNNB1 (β-catenin) or mutational inactivation of APC and Axin1 genes in some tumors. However, there are many tumors that display β-catenin accumulation in the absence of a mutation in these genes. Thus, there must be additional sources for aberrant β-catenin accumulation in cancer cells. Here, we provide experimental evidence that wild-type β-catenin accumulates in hepatocellular carcinoma (HCC) cells in association with mutational inactivation of p53 gene. We also show that worldwide p53 and β-catenin mutation rates are inversely correlated in HCC. These data suggest that inactivation of p53 is an important cause of aberrant accumulation of β-catenin in cancer cells.Englishβ-cateninHepatocellular carcinomaMutationp53wnt pathwaybeta cateninprotein p53articlecarcinoma cellclinical articlecontrolled studycorrelation analysisgene inactivationgene mutationhumanhuman cellliver cell carcinomapriority journalbeta CateninCytoskeletal ProteinsHumansLiver NeoplasmsMutationTrans-ActivatorsTumor Cells, CulturedTumor Suppressor Protein p53Article10.1038/sj.onc.1205919