ArticleNature communications2015
Tumour suppressor TRIM33 targets nuclear β-catenin degradation.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed.
- Suppression of TRIM33 and SMAD4 Indicates a Possible Tumor-Suppressive Role in Esophageal Squamous Cell Carcinoma.Digestive diseases and sciences · 2026Article
- Transcriptional intermediary factor 1 gamma-based multitarget gene therapeutic strategy for triple-negative breast cancer.Signal transduction and targeted therapy · 2026Article
- Positive selection screen identifies natural product β-catenin inactivators.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- TIF1γ holds the line against regulatory T cell plasticity.Nature immunology · 2026Article
- TIF1γ regulates stability of regulatory T cells during inflammation.Nature immunology · 2026Article
- TRIM33 Reverses Cisplatin Resistance in Non-Small Cell Lung Cancer by Regulating the PI3K/AKT Pathway via Ubiquitination-Mediated Degradation of LPCAT1.World journal of oncology · 2026Article
- Restoring the tumour mechanophenotype of vocal fold cancer reverts its malignant properties.Nature materials · 2026Article
- UVB-induced genotoxic stress activates the DNA damage response and innate immune pathways in sea urchin coelomocytes.Frontiers in immunology · 2026Article
- Targeting β-catenin: PROTACs and precision degraders for Wnt-driven cancers.Frontiers in oncology · 2026Review
- Nuclear β-catenin: molecular regulation, challenges and therapeutic opportunities.Cell communication and signaling : CCS · 2025Review
- Restoration of BAP1 activity via base editing suppresses anchorage-independent survival in kidney cancer.Cancer cell international · 2025Article
- STUPPIT is a proximity labeling tool for labeling intermediary proteins that bridge two non-interacting proteins.PLoS biology · 2025Article
- A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies.Cancer cell · 2025Article
- Clinical Profile and Outcomes in Anti-TIF1γ Positive Idiopathic Inflammatory Myositis Patients: A Greek Cohort Study.Mediterranean journal of rheumatology · 2025Article
- IGF1R activates FOXP3-β-catenin signaling to promote breast cancer development.Breast cancer research and treatment · 2025Article
- Inhibition of SCFCommunications biology · 2025Article
- TRIM6 Promotes Cell Cycle and Growth by Modulating p53 Signaling Pathway in Lung Adenocarcinoma.International journal of general medicine · 2025Article
- Convergent Evolution Associated with the Loss of Developmental Diapause May Promote Extended Lifespan in Bees.Genome biology and evolution · 2024Article
- CLIP170 enhancing FOSL1 expression via attenuating ubiquitin-mediated degradation of β-catenin drives renal cell carcinoma progression.Cellular and molecular life sciences : CMLS · 2024Article
- TRIM33 promotes glycolysis through regulating P53 K48-linked ubiquitination to promote esophageal squamous cell carcinoma growth.Cell death & disease · 2024Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Aberrant activation of β-catenin in the nucleus has been implicated in a variety of human cancers, but the fate of nuclear β-catenin is unknown. Here we demonstrate that the tripartite motif-containing protein 33 (TRIM33), acting as an E3 ubiquitin ligase, reduces the abundance of nuclear β-catenin protein. TRIM33-mediated β-catenin is destabilized and is GSK-3β or β-TrCP independent. TRIM33 interacts with and ubiquitylates nuclear β-catenin. Moreover, protein kinase Cδ, which directly phosphorylates β-catenin at Ser715, is required for the TRIM33-β-catenin interaction. The function of TRIM33 in suppressing tumour cell proliferation and brain tumour development depends on TRIM33-promoted β-catenin degradation. In human glioblastoma specimens, endogenous TRIM33 levels are inversely correlated with β-catenin. In summary, our findings identify TRIM33 as a tumour suppressor that can abolish tumour cell proliferation and tumorigenesis by degrading nuclear β-catenin. This work suggests a new therapeutic strategy against human cancers caused by aberrant activation of β-catenin.
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