ArticleThe Journal of pathology2018
αE-catenin is a candidate tumor suppressor for the development of E-cadherin-expressing lobular-type breast cancer.
Article in The Journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Toward targeted therapeutics for lobular breast cancer.The Journal of clinical investigation · 2026Review
- Article
- Two δ-catenins, plakophilin 4 and p120, promote formation of distinct types of adherens junctions.The Journal of cell biology · 2026Article
- Circ_0074158 and QKI6: A regulatory axis for PD-L1 ubiquitination and immune evasion in NSCLC.Cancer immunology, immunotherapy : CII · 2025Article
- Afadin loss induces breast cancer metastasis through destabilisation of E-cadherin to F-actin linkage.The Journal of pathology · 2025Article
- E-cadherin staining in the diagnosis of lobular versus ductal neoplasms of the breast: the emperor has no clothes.Histopathology · 2025Review
- Review
- Unraveling complexity and leveraging opportunities in uncommon breast cancer subtypes.NPJ breast cancer · 2025Review
- Molecular Basis of Breast Tumor Heterogeneity.Advances in experimental medicine and biology · 2025Review
- Insights into E-Cadherin Impairment inInternational journal of molecular sciences · 2024Article
- Microenvironment-induced restoration of cohesive growth associated with focal activation of P-cadherin expression in lobular breast carcinoma metastatic to the colon.The journal of pathology. Clinical research · 2024Article
- Genomic and epigenomic basis of breast invasive lobular carcinomas lacking CDH1 genetic alterations.NPJ precision oncology · 2024Article
- α-Catenin acetylation is essential for its stability and blocks its tumor suppressor effects in breast cancer through Yap1.Cancer gene therapy · 2023Article
- Review
- Genomic profiling and pre-clinical modelling of breast cancer leptomeningeal metastasis reveals acquisition of a lobular-like phenotype.Nature communications · 2023Article
- Uncommon invasive lobular carcinoma with papillary architecture-clinicopathologic and molecular characterization with review of the literature.Virchows Archiv : an international journal of pathology · 2023Review
- Anoikis resistance--protagonists of breast cancer cells survive and metastasize after ECM detachment.Cell communication and signaling : CCS · 2023Review
- CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling.Breast cancer research : BCR · 2023Article
- The Role of CTNNA1 in Malignancies: An Updated Review.Journal of Cancer · 2023Review
- Hereditary Diffuse Gastric Cancer: A 2022 Update.Journal of personalized medicine · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Although mutational inactivation of E-cadherin (CDH1) is the main driver of invasive lobular breast cancer (ILC), approximately 10-15% of all ILCs retain membrane-localized E-cadherin despite the presence of an apparent non-cohesive and invasive lobular growth pattern. Given that ILC is dependent on constitutive actomyosin contraction for tumor development and progression, we used a combination of cell systems and in vivo experiments to investigate the consequences of α-catenin (CTNNA1) loss in the regulation of anchorage independence of non-invasive breast carcinoma. We found that inactivating somatic CTNNA1 mutations in human breast cancer correlated with lobular and mixed ducto-lobular phenotypes. Further, inducible loss of α-catenin in mouse and human E-cadherin-expressing breast cancer cells led to atypical localization of E-cadherin, a rounded cell morphology, and anoikis resistance. Pharmacological inhibition experiments subsequently revealed that, similar to E-cadherin-mutant ILC, anoikis resistance induced by α-catenin loss was dependent on Rho/Rock-dependent actomyosin contractility. Finally, using a transplantation-based conditional mouse model, we demonstrate that inducible inactivation of α-catenin instigates acquisition of lobular features and invasive behavior. We therefore suggest that α-catenin represents a bona fide tumor suppressor for the development of lobular-type breast cancer and as such provides an alternative event to E-cadherin inactivation, adherens junction (AJ) dysfunction, and subsequent constitutive actomyosin contraction. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
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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.