p53 mutation as a source of aberrant β-catenin accumulation in cancer cells
dc.citation.epage | 7980 | en_US |
dc.citation.issueNumber | 52 | en_US |
dc.citation.spage | 7971 | en_US |
dc.citation.volumeNumber | 21 | en_US |
dc.contributor.author | Cagatay, T. | en_US |
dc.contributor.author | Ozturk, M. | en_US |
dc.date.accessioned | 2016-02-08T10:31:57Z | |
dc.date.available | 2016-02-08T10:31:57Z | |
dc.date.issued | 2002 | en_US |
dc.department | Department of Molecular Biology and Genetics | en_US |
dc.description.abstract | β-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.description.provenance | Made available in DSpace on 2016-02-08T10:31:57Z (GMT). No. of bitstreams: 1 bilkent-research-paper.pdf: 70227 bytes, checksum: 26e812c6f5156f83f0e77b261a471b5a (MD5) Previous issue date: 2002 | en |
dc.identifier.doi | 10.1038/sj.onc.1205919 | en_US |
dc.identifier.issn | 0950-9232 | |
dc.identifier.uri | http://hdl.handle.net/11693/24623 | |
dc.language.iso | English | en_US |
dc.relation.isversionof | http://dx.doi.org/10.1038/sj.onc.1205919 | en_US |
dc.source.title | Oncogene | en_US |
dc.subject | β-catenin | en_US |
dc.subject | Hepatocellular carcinoma | en_US |
dc.subject | Mutation | en_US |
dc.subject | p53 | en_US |
dc.subject | wnt pathway | en_US |
dc.subject | beta catenin | en_US |
dc.subject | protein p53 | en_US |
dc.subject | article | en_US |
dc.subject | carcinoma cell | en_US |
dc.subject | clinical article | en_US |
dc.subject | controlled study | en_US |
dc.subject | correlation analysis | en_US |
dc.subject | gene inactivation | en_US |
dc.subject | gene mutation | en_US |
dc.subject | human | en_US |
dc.subject | human cell | en_US |
dc.subject | liver cell carcinoma | en_US |
dc.subject | priority journal | en_US |
dc.subject | beta Catenin | en_US |
dc.subject | Cytoskeletal Proteins | en_US |
dc.subject | Humans | en_US |
dc.subject | Liver Neoplasms | en_US |
dc.subject | Mutation | en_US |
dc.subject | Trans-Activators | en_US |
dc.subject | Tumor Cells, Cultured | en_US |
dc.subject | Tumor Suppressor Protein p53 | en_US |
dc.title | p53 mutation as a source of aberrant β-catenin accumulation in cancer cells | en_US |
dc.type | Article | en_US |
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