ArticleNature communications2019
Rebalancing of actomyosin contractility enables mammary tumor formation upon loss of E-cadherin.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Trial
- Multidimensional Cellular Micro-Compartments to Model Invasive Lobular Carcinoma Dormancy.Advanced healthcare materials · 2026Article
- Mapping the genetic landscape of hereditary diffuse-type gastric cancer progression.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Article
- Non-canonical EGFR signaling promotes MAPK-dependent extrusion of epithelial cells.Journal of cell science · 2025Article
- TP63 mediates the generation of tumour-specific chromatin loops that underlie MYC activation in radiation-induced tumorigenesis.Nature communications · 2025Article
- Gastrointestinal metastasis from invasive lobular carcinoma following breast cancer treatment: A case report.World journal of clinical cases · 2025Article
- Article
- Intercellular contractile force attenuates chemosensitivity through Notch-MVP-mediated nuclear drug export.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- E-Cadherin-Mediated Cell-Cell Adhesion and Invasive Lobular Breast Cancer.Advances in experimental medicine and biology · 2025Review
- Intelligent gold nanocluster for effective treatment of malignant tumor via tumor-specific photothermal-chemodynamic therapy with AIE guidance.National science review · 2024Article
- The role and mechanism of compressive stress in tumor.Frontiers in oncology · 2024Review
- Genomic profiling and pre-clinical modelling of breast cancer leptomeningeal metastasis reveals acquisition of a lobular-like phenotype.Nature communications · 2023Article
- MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer.The Journal of experimental medicine · 2023Article
- Volume imaging to interrogate cancer cell-tumor microenvironment interactions in space and time.Frontiers in immunology · 2023Review
- E-Cadherin Expression Distinguishes Mouse from Human Hematopoiesis in the Basophil and Erythroid Lineages.Biomolecules · 2022Article
- Amoeboid migration in health and disease: Immune responsesFrontiers in cell and developmental biology · 2022Review
- Exploiting differential effects of actomyosin contractility to control cell sorting among breast cancer cells.Molecular biology of the cell · 2021Article
- Review
- Canonical Wnt: a safeguard and threat for erythropoiesis.Blood advances · 2021Review
- Lobular Breast Cancer: Histomorphology and Different Concepts of a Special Spectrum of Tumors.Cancers · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E-cadherin (CDH1) is a master regulator of epithelial cell adherence junctions and a well-established tumor suppressor in Invasive Lobular Carcinoma (ILC). Intriguingly, somatic inactivation of E-cadherin alone in mouse mammary epithelial cells (MMECs) is insufficient to induce tumor formation. Here we show that E-cadherin loss induces extrusion of luminal MMECs to the basal lamina. Remarkably, E-cadherin-deficient MMECs can breach the basal lamina but do not disseminate into the surrounding fat pad. Basal lamina components laminin and collagen IV supported adhesion and survival of E-cadherin-deficient MMECs while collagen I, the principle component of the mammary stromal micro-environment did not. We uncovered that relaxation of actomyosin contractility mediates adhesion and survival of E-cadherin-deficient MMECs on collagen I, thereby allowing ILC development. Together, these findings unmask the direct consequences of E-cadherin inactivation in the mammary gland and identify aberrant actomyosin contractility as a critical barrier to ILC formation.
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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.