The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
A Nonapoptotic Cell Death Process, Entosis, that Occurs by Cell-in-Cell Invasion
Open accessAbstract
Epithelial cells require attachment to extracellular matrix (ECM) to suppress an apoptotic cell death program termed anoikis. Here we describe a nonapoptotic cell death program in matrix-detached cells that is initiated by a previously unrecognized and unusual process involving the invasion of one cell into another, leading to a transient state in which a live cell is contained within a neighboring host cell. Live internalized cells are either degraded by lysosomal enzymes or released. We term this cell internalization process entosis and present evidence for entosis as a mechanism underlying the commonly observed "cell-in-cell" cytological feature in human cancers. Further we propose that entosis is driven by compaction force associated with adherens junction formation in the absence of integrin engagement and may represent an intrinsic tumor suppression mechanism for cells that are detached from ECM.
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In the citing paper
“Entosis is a live-cell engulfment pathway occurring between two neighbouring cells, one of which will be actively engulfed by the other to form a ‘cell-in-cell’ structure [35].”
From LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy (2012) · cites this paper as [35]
In the citing paper
“Entosis is mainly triggered by the detachment of epithelial cells from the extracellular matrix and consequent loss of integrin signaling [263, 694]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [694]
In the citing paper
“Once engulfed, entotic cells are often eliminated by a RCD subroutine that occurs independently of BCL2 proteins and caspases [694, 704], but relies (at least in part) on a specific autophagy-related process commonly known as LC3-associated phagocytosis (LAP) [509, 705, 706].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [694]
In the citing paper
“abrogation of entosis by a chemical ROCK inhibitor reportedly favors the anchorage-independent growth of malignant cells [694].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [694]
In the citing paper
“the uptake of entotic cells is an integrin-independent process promoted by the formation of junctions between engulfing and entotic cells that involve the adhesion proteins cadherin 1 (CDH1; also known as E-cadherin) and catenin alpha 1 (CTNNA1) [694, 699].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [694]
In the citing paper
“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 [694]
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Metadata
- Authors
- Overholtzer, M., Mailleux, A. A., Mouneimne, G., Normand, G., Schnitt, S. J., King, R. W., Cibas, E. S., & Brugge, J. S.
- Affiliations
- Harvard University (US)
- Beth Israel Deaconess Medical Center (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Brugge, Joan S.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2007-11
- Volume
- 131
- Issue
- 5
- Pages
- 966-979
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2112497627
- Cited by
- 748
- References
- 38
- Citations by year
- 2026: 30 · 2025: 50 · 2024: 61 · 2023: 63 · 2022: 44 · 2021: 55 · 2020: 43 · 2019: 54 · 2018: 51 · 2017: 44 · 2016: 28 · 2015: 38 · 2014: 23 · 2013: 39 · 2012: 31
- FWCI
- 8.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2121 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (T32-CA 09361, CA 089393, T32CA009361, CA080111, P01CA080111, P50CA089393)
- National Institute of General Medical Sciences (GM66492)
- 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 › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- entosis, non-apoptotic cell death, anoikis, extracellular matrix detachment, cellular internalization, lysosomal degradation, adherens junctions, tumor suppression, epithelial cells, tumor cytology
- MeSH terms
- Actins, Autophagy, Breast Neoplasms, Carcinoma, Cell Adhesion, Cell Communication, Extracellular Matrix, Humans, Lysosomes, Models, Biological, Tumor Cells, Cultured, Cadherins, Apoptosis, rho GTP-Binding Proteins, Adherens Junctions, Myosin Type II, rho-Associated Kinases
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