β-Catenin regulates expression of cyclin D1 in colon carcinoma cells
Abstract
Mutations in the adenomatous polyposis coli (APC) tumour-suppressor gene occur in most human colon cancers. Loss of functional APC protein results in the accumulation of beta-catenin. Mutant forms of beta-catenin have been discovered in colon cancers that retain wild-type APC genes, and also in melanomas, medulloblastomas, prostate cancer and gastric and hepatocellular carcinomas. The accumulation of beta-catenin activates genes that are responsive to transcription factors of the TCF/LEF family, with which beta-catenin interacts. Here we show that beta-catenin activates transcription from the cyclin D1 promoter, and that sequences within the promoter that are related to consensus TCF/LEF-binding sites are necessary for activation. The oncoprotein p21ras further activates transcription of the cyclin D1 gene, through sites within the promoter that bind the transcriptional regulators Ets or CREB. Cells expressing mutant beta-catenin produce high levels of cyclin D1 messenger RNA and protein constitutively. Furthermore, expression of a dominant-negative form of TCF in colon-cancer cells strongly inhibits expression of cyclin D1 without affecting expression of cyclin D2, cyclin E, or cyclin-dependent kinases 2, 4 or 6. This dominant-negative TCF causes cells to arrest in the G1 phase of the cell cycle; this phenotype can be rescued by expression of cyclin D1 under the cytomegalovirus promoter. Abnormal levels of beta-catenin may therefore contribute to neoplastic transformation by causing accumulation of cyclin D1.
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Wnt/β-catenin signaling controls the G1/S transition.
“The Wnt/β-catenin signaling pathway is one of the mechanisms known to control G1/S transition (35–38).”
From Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade (2022) · cites this paper as [37]
When WNT ligands are present, β-catenin degradation is impeded, causing its nuclear translocation and subsequent binding to T-cell factor (TCF), which results in the transcriptional activation of their target genes.
“When WNT ligands are present, β-catenin degradation is impeded, causing its nuclear translocation and subsequent binding to T-cell factor (TCF), which results in the transcriptional activation of their target genes.443,445,446”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [446]
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- Authors
- Tetsu, O., & McCormick, F.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- McCormick, Frank
- Venue
- Nature
- Published
- 1999-04
- Volume
- 398
- Issue
- 6726
- Pages
- 422-426
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1554815317
- Cited by
- 3,601
- References
- 28
- Citations by year
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- FWCI
- 67.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- β-catenin, cyclin D1, colon cancer, APC gene, TCF/LEF transcription factors, transcriptional activation, p21ras, ETS transcription factors, CREB, G1 cell cycle arrest, oncogenic transformation, cyclin-dependent kinases
- MeSH terms
- Binding Sites, Cell Division, Colonic Neoplasms, Cytoskeletal Proteins, HeLa Cells, Humans, Luciferases, Promoter Regions, Genetic, Recombinant Fusion Proteins, Transcription Factors, Transcription, Genetic, Tumor Cells, Cultured, Blotting, Western, Trans-Activators, Gene Expression Regulation, Neoplastic, G1 Phase, Mutagenesis, Site-Directed, Consensus Sequence, ras Proteins, Cyclin D1, Reverse Transcriptase Polymerase Chain Reaction, beta Catenin, TCF Transcription Factors, Transcription Factor 7-Like 2 Protein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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