ArticleMolecular and cellular biology2001
Down-regulation of beta-catenin by activated p53.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 227 citations in OpenAlex.
- The p53-PA200 Feedback Loop Modulates Age-Dependent Tumorigenesis.International journal of molecular sciences · 2026Article
- Reciprocal compensation of caspase-2 and p53 regulates the DNA damage response in HCT116 colon cancer cells.The Journal of biological chemistry · 2026Article
- Exploring the oncogenic mechanism of plasmacytoma variant translocation 1 (PVT1) gene in solid cancers; emphasis on microRNA regulation pathways.Cancer cell international · 2026Review
- Junction Plakoglobin - A Dual-Role Player in Cancer Biology.International journal of surgery (London, England) · 2025Review
- Reciprocal and non-reciprocal effects of clinically relevant SETBP1 protein dosage changes.Human molecular genetics · 2025Article
- Therapeutic potential of flavonoids in gastrointestinal cancer: Focus on signaling pathways and improvement strategies (Review).Molecular medicine reports · 2025Review
- GATA6 Amplification Is Associated With Improved Survival in TP53-Mutated Unresectable Pancreatic Cancer.Pancreas · 2025Article
- PARInternational journal of molecular sciences · 2025Article
- Review
- The Effect of Ionising Radiation on the Properties of Tumour-Derived Exosomes and Their Ability to Modify the Biology of Non-Irradiated Breast Cancer Cells-An In Vitro Study.International journal of molecular sciences · 2025Article
- The crosstalk of Wnt/β-catenin signaling and p53 in acute kidney injury and chronic kidney disease.Kidney research and clinical practice · 2024Article
- Unraveling the chemotherapeutic potential of taxifolin ruthenium-p-cymene complex in breast carcinoma: Insights into AhR signaling pathway in vitro and in vivo.Translational oncology · 2024Article
- Inhibition of TBL1 cleavage alleviates doxorubicin-induced cardiomyocytes death by regulating the Wnt/β-catenin signal pathway.Cardiovascular research · 2024Article
- Wnt signaling modulates the response to DNA damage in the Drosophila wing imaginal disc by regulating the EGFR pathway.PLoS biology · 2024Article
- The role of proteasomes in tumorigenesis.Genes & diseases · 2024Review
- Cancer Mutations Converge on a Collection of Protein Assemblies to Predict Resistance to Replication Stress.Cancer discovery · 2024Article
- ZMIZ2 facilitates hepatocellular carcinoma progression via LEF1 mediated activation of Wnt/β-catenin pathway.Experimental hematology & oncology · 2024Article
- β-catenin inhibitors in cancer therapeutics: intricacies and way forward.Bioengineered · 2023Review
- Estimation of genomic and mitochondrial DNA integrity in the renal tissue of mice administered with acrylamide and titanium dioxide nanoparticles.Scientific reports · 2023Article
- Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
beta-Catenin is a cytoplasmic protein that participates in the assembly of cell-cell adherens junctions by binding cadherins to the actin cytoskeleton. In addition, it is a key component of the Wnt signaling pathway. Activation of this pathway triggers the accumulation of beta-catenin in the nucleus, where it activates the transcription of target genes. Abnormal accumulation of beta-catenin is characteristic of various types of cancer and is caused by mutations either in the adenomatous polyposis coli protein, which regulates beta-catenin degradation, or in the beta-catenin molecule itself. Aberrant accumulation of beta-catenin in tumors is often associated with mutational inactivation of the p53 tumor suppressor. Here we show that overexpression of wild-type p53, by either transfection or DNA damage, down-regulates beta-catenin in human and mouse cells. This effect was not obtained with transcriptionally inactive p53, including a common tumor-associated p53 mutant. The reduction in beta-catenin level was accompanied by inhibition of its transactivation potential. The inhibitory effect of p53 on beta-catenin is apparently mediated by the ubiquitin-proteasome system and requires an active glycogen synthase kinase 3beta (GSK3beta). Mutations in the N terminus of beta-catenin which compromise its degradation by the proteasomes, overexpression of dominant-negative DeltaF-beta-TrCP, or inhibition of GSKbeta activity all rendered beta-catenin resistant to down-regulation by p53. These findings support the notion that there will be a selective pressure for the loss of wild-type p53 expression in cancers that are driven by excessive accumulation of beta-catenin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.