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Stabilization of beta-catenin by genetic defects in melanoma cell lines.
- Source :
-
Science (New York, N.Y.) [Science] 1997 Mar 21; Vol. 275 (5307), pp. 1790-2. - Publication Year :
- 1997
-
Abstract
- Signal transduction by beta-catenin involves its posttranslational stabilization and downstream coupling to the Lef and Tcf transcription factors. Abnormally high amounts of beta-catenin were detected in 7 of 26 human melanoma cell lines. Unusual messenger RNA splicing and missense mutations in the beta-catenin gene (CTNNB1) that result in stabilization of the protein were identified in six of the lines, and the adenomatous polyposis coli tumor suppressor protein (APC) was altered or missing in two others. In the APC-deficient cells, ectopic expression of wild-type APC eliminated the excess beta-catenin. Cells with stabilized beta-catenin contained a constitutive beta-catenin-Lef-1 complex. Thus, genetic defects that result in up-regulation of beta-catenin may play a role in melanoma progression.
- Subjects :
- Adenomatous Polyposis Coli Protein
Animals
Cell Line
Cytoskeletal Proteins chemistry
Cytoskeletal Proteins metabolism
DNA-Binding Proteins metabolism
Humans
Lymphoid Enhancer-Binding Factor 1
Melanoma metabolism
Mice
Mutation
Point Mutation
RNA Splicing
RNA, Messenger genetics
RNA, Neoplasm genetics
Transcription Factors metabolism
Transfection
Tumor Cells, Cultured
Up-Regulation
beta Catenin
Cytoskeletal Proteins genetics
Gene Expression Regulation, Neoplastic
Genes, APC
Melanoma genetics
Trans-Activators
Subjects
Details
- Language :
- English
- ISSN :
- 0036-8075
- Volume :
- 275
- Issue :
- 5307
- Database :
- MEDLINE
- Journal :
- Science (New York, N.Y.)
- Publication Type :
- Academic Journal
- Accession number :
- 9065403
- Full Text :
- https://doi.org/10.1126/science.275.5307.1790