ArticleCell research2014
Induction of entosis by epithelial cadherin expression.
Article in Cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
108 citing papers in PubMed, 2 syntheses or guidelines pooled it, 148 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- A bibliometric and visualization analysis of entosis research from 2007 to 2024.Frontiers in oncology · 2024Pooled it
- Metabolic hallmarks of regulated cell death.Cell research · 2026Review
- ARHGAP36 imposes a bifurcate activation of adherens junction and actomyosin to promote entosis.Cell death and differentiation · 2026Article
- Leveraging Deep Learning to Construct a Programmed Cell Death-Driven Prognostic Signature in Acute Myeloid Leukemia.Current issues in molecular biology · 2026Article
- Review
- Construction and validation of a cell-in-cell related prognostic signature for hepatocellular carcinoma.Discover oncology · 2025Article
- Molecular Dynamics of Trogocytosis and Other Contact-Dependent Cell Trafficking Mechanisms in Tumor Pathogenesis.Cancers · 2025Review
- ROCK signaling is involved in the entosis of both nonepithelial and epithelial tumors, whereas N‑cadherin is involved in the entosis of nonepithelial tumors.Experimental and therapeutic medicine · 2025Article
- CDC25A inhibition sensitizes melanoma cells to doxorubicin and NK cell therapy.Cell death & disease · 2025Article
- CDH-3/Cadherin, YAP-1/YAP and EGL-44/TEAD promote SYX-2/Syntaxin and EFF-1 fusogen-mediated phagosome closure.bioRxiv : the preprint server for biology · 2025Article
- Identification of the entosis-related prognostic signature and tumour microenvironment in hepatocellular carcinoma on the basis of bioinformatics analysis and experimental validation.Clinical and experimental medicine · 2025Article
- CT45A1-mediated MLC2 (MYL9) phosphorylation promotes natural killer cell resistance and outer cell fate in a cell-in-cell structure, potentiating the progression of microsatellite instability-high colorectal cancer.Molecular oncology · 2025Article
- Colorectal cancer stem cells develop NK cell resistance via homotypic cell-in-cell structures suppressed by Stathmin1.Theranostics · 2025Article
- Case Report: Comparison different response after neoadjuvant chemotherapy of the breast with cell-in-cell-report of two cases.Frontiers in medicine · 2025Article
- Entosis in Health and Disease.Advances in experimental medicine and biology · 2025Review
- Advances in non-apoptotic regulated cell death: implications for malignant tumor treatment.Frontiers in oncology · 2025Review
- Cell hiding in colorectal cancer: correlation with response to chemotherapy in vitro and in vivo.Scientific reports · 2024Article
- Review
- Entosis: the core mechanism and crosstalk with other cell death programs.Experimental & molecular medicine · 2024Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 2 countries.
Funding
Abstract
Cell engulfment typically targets dead or dying cells for clearance from metazoan tissues. However, recent evidence demonstrates that live cells can also be targeted and that engulfment can cause cell death. Entosis is one mechanism proposed to mediate the engulfment and killing of live tumor cells by their neighbors, an activity often referred to as cell cannibalism. Here we report that the expression of exogenous epithelial cadherin proteins (E- or P-cadherin) in human breast tumor cells lacking endogenous expression of epithelial cadherins induces entosis and inhibits transformed growth. Entosis induced by cadherin expression is associated with the polarized distribution of Rho and Rho-kinase (ROCK) activity within entotic cells, which is dependent on p190A RhoGAP activity. ROCK inhibition or downregulation of p190A RhoGAP expression reduces entosis and increases the transformed growth of epithelial cadherin-expressing tumor cells. These data define new cell systems for the study of entosis, and identify entosis as a mechanism of cell cannibalism that is induced by the establishment of epithelial adhesion and inhibits transformed growth.
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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.