ArticleNature cell biology2014
α-catenin acts as a tumour suppressor in E-cadherin-negative basal-like breast cancer by inhibiting NF-κB signalling.
Article in Nature cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 94 citations in OpenAlex.
- Krüppel-like factor 10 promotes the progression of breast cancer by activating canonical NF-κB signaling.iScience · 2026Article
- LAR1 promotes breast carcinogenesis by activating NF-κB signaling pathway through binding and enhancing APOC1 expression.iScience · 2026Article
- The role of SUMOylation in epithelial-mesenchymal transition.Journal of molecular medicine (Berlin, Germany) · 2025Review
- [Integrative transcriptomics-metabolomics approach to identify metabolic pathways regulated by glutamine synthetase activity].Se pu = Chinese journal of chromatography · 2025Article
- α-Catenin acetylation is essential for its stability and blocks its tumor suppressor effects in breast cancer through Yap1.Cancer gene therapy · 2023Article
- Review
- Anoikis resistance--protagonists of breast cancer cells survive and metastasize after ECM detachment.Cell communication and signaling : CCS · 2023Review
- α-catenin interaction with YAP/FoxM1/TEAD-induced CEP55 supports liver cancer cell migration.Cell communication and signaling : CCS · 2023Article
- Transcriptomic analysis provides insight into the mechanism of IKKβ-mediated suppression of HPV18E6-induced cellular abnormalities.G3 (Bethesda, Md.) · 2023Article
- Cadherins and catenins in cancer: connecting cancer pathways and tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- The Role of CTNNA1 in Malignancies: An Updated Review.Journal of Cancer · 2023Review
- α-Catenin links integrin adhesions to F-actin to regulate ECM mechanosensing and rigidity dependence.The Journal of cell biology · 2022Article
- Molecular Mechanisms and Potential Rationale of Immunotherapy in Peritoneal Metastasis of Advanced Gastric Cancer.Biomedicines · 2022Review
- Functional impact of multi-omic interactions in breast cancer subtypes.Frontiers in genetics · 2022Article
- YB1 regulates miR-205/200b-ZEB1 axis by inhibiting microRNA maturation in hepatocellular carcinoma.Cancer communications (London, England) · 2021Article
- Apatinib suppresses the migration, invasion and angiogenesis of hepatocellular carcinoma cells by blocking VEGF and PI3K/AKT signaling pathways.Molecular medicine reports · 2021Article
- Catenin α 1 mutations cause familial exudative vitreoretinopathy by overactivating Norrin/β-catenin signaling.The Journal of clinical investigation · 2021Article
- SUMOylation Wrestles With the Occurrence and Development of Breast Cancer.Frontiers in oncology · 2021Review
- Tumor suppressive function of Matrin 3 in the basal-like breast cancer.Biological research · 2020Article
- Can NF-κB Be Considered a Valid Drug Target in Neoplastic Diseases? Our Point of View.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Basal-like breast cancer is a highly aggressive tumour subtype associated with poor prognosis. Aberrant activation of NF-κB signalling is frequently found in triple-negative basal-like breast cancer cells, but the cause of this activation has remained elusive.Here we report that α-catenin functions as a tumour suppressor in E-cadherin-negative basal-like breast cancer cells by inhibiting NF-κB signalling. Mechanistically, α-catenin interacts with the IκBα protein, and stabilizes IκBα by inhibiting its ubiquitylation and its association with the proteasome. This stabilization in turn prevents nuclear localization of RelA and p50, leading to decreased expression of TNF-α, IL-8 and RelB. In human breast cancer, CTNNA1 expression is specifically downregulated in the basal-like subtype, correlates with clinical outcome and inversely correlates with TNF and RELB expression. Taken together, these results uncover a previously undescribed mechanism by which the NF-κB pathway is activated in E-cadherin-negative basal-like breast cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.