p53 mutation as a source of aberrant β-catenin accumulation in cancer cells

dc.citation.epage7980en_US
dc.citation.issueNumber52en_US
dc.citation.spage7971en_US
dc.citation.volumeNumber21en_US
dc.contributor.authorCagatay, T.en_US
dc.contributor.authorOzturk, M.en_US
dc.date.accessioned2016-02-08T10:31:57Z
dc.date.available2016-02-08T10:31:57Z
dc.date.issued2002en_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractβ-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.en_US
dc.identifier.doi10.1038/sj.onc.1205919en_US
dc.identifier.issn0950-9232
dc.identifier.urihttp://hdl.handle.net/11693/24623
dc.language.isoEnglishen_US
dc.relation.isversionofhttp://dx.doi.org/10.1038/sj.onc.1205919en_US
dc.source.titleOncogeneen_US
dc.subjectβ-cateninen_US
dc.subjectHepatocellular carcinomaen_US
dc.subjectMutationen_US
dc.subjectp53en_US
dc.subjectwnt pathwayen_US
dc.subjectbeta cateninen_US
dc.subjectprotein p53en_US
dc.subjectarticleen_US
dc.subjectcarcinoma cellen_US
dc.subjectclinical articleen_US
dc.subjectcontrolled studyen_US
dc.subjectcorrelation analysisen_US
dc.subjectgene inactivationen_US
dc.subjectgene mutationen_US
dc.subjecthumanen_US
dc.subjecthuman cellen_US
dc.subjectliver cell carcinomaen_US
dc.subjectpriority journalen_US
dc.subjectbeta Cateninen_US
dc.subjectCytoskeletal Proteinsen_US
dc.subjectHumansen_US
dc.subjectLiver Neoplasmsen_US
dc.subjectMutationen_US
dc.subjectTrans-Activatorsen_US
dc.subjectTumor Cells, Cultureden_US
dc.subjectTumor Suppressor Protein p53en_US
dc.titlep53 mutation as a source of aberrant β-catenin accumulation in cancer cellsen_US
dc.typeArticleen_US
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