Induction of entosis by epithelial cadherin expression
Open accessAbstract
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.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Entotic cell death has been documented in several human neoplasms, presumably operating as an oncosuppressor mechanism.
“Entotic cell death has been documented in several human neoplasms, presumably operating as an oncosuppressor mechanism [694, 695, 701, 709, 710].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [701]
Forced overexpression of RHOA or ROCK1 plus ROCK2 enables internalization of entotic cells by epithelial CDH1-expressing cells.
“forced overexpression of RHOA or ROCK1 plus ROCK2 enables the internalization of entotic cells by epithelial CDH1-expressing cells [701].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [701]
Administration of exogenous CDH1 promotes entosis among CDH1-deficient breast cancer cells.
“the administration of exogenous CDH1 promotes entosis among CDH1-deficient breast cancer cells”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [701]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 46 · Cited by 148
- Authors
- Sun, Q., Cibas, E. S., Huang, H., Hodgson, L., & Overholtzer, M.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Brigham and Women's Hospital (US)
- Capital Medical University (CN)
- Albert Einstein College of Medicine (US)
- Corresponding author
- Sun, Qiang
- Overholtzer, Michael
- Venue
- Cell Research
- Published
- 2014-10-24
- Volume
- 24
- Issue
- 11
- Pages
- 1288-1298
- ISSN
- 1001-0602 (ISSN-L)
- 1748-7838
- PMC
- PMC4220160
- OpenAlex
- W2043133007
- Cited by
- 148
- References
- 46
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 11 · 2023: 17 · 2022: 21 · 2021: 16 · 2020: 11 · 2019: 15 · 2018: 14 · 2017: 9 · 2016: 6 · 2015: 10 · 2014: 2
- FWCI
- 3.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Memorial Sloan-Kettering Cancer Center
- Geoffrey Beene Cancer Research Center
- National Natural Science Foundation of China (81472588)
- National Key Research and Development Program of China (2015CB553704)
- National Cancer Institute (R01CA154649, CA154649, P30CA008748)
- National Institute of General Medical Sciences (GM09312, R01GM093121)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- entosis, E-cadherin, P-cadherin, cell cannibalism, cell engulfment, Rho kinase, epithelial cell adhesion, breast tumor cells, cell death
- MeSH terms
- Actomyosin, Humans, Myosins, Repressor Proteins, Down-Regulation, Cadherins, Microscopy, Confocal, Guanine Nucleotide Exchange Factors, rhoA GTP-Binding Protein, RNA Interference, RNA, Small Interfering, Cell Line, Tumor, rho-Associated Kinases, Entosis, Time-Lapse Imaging, MCF-7 Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
