Entosis: The core mechanism and crosstalk with other cell death programs Review


Authors: Kim, S.; Lee, D.; Kim, S. E.; Overholtzer, M.
Review Title: Entosis: The core mechanism and crosstalk with other cell death programs
Abstract: Cell death, a complex process, can happen through various mechanisms, including entosis. Entosis, first identified as a non-apoptotic cell death program, involves one cell engulfing another, causing the death of the internalized cell. However, the exact molecular mechanisms and factors controlling entosis are unclear. In this study, the authors review recent findings uncovering the molecular regulation of entosis and dicuss its potential implications in cancer. They discuss how entosis is controlled by a network of regulations involving cell adhesion, the RhoA–ROCK signaling pathway, and actomyosin contraction. Interestingly, entosis can occur alongside other cell death forms in populations, suggesting it may influence how cell groups respond to stress. The study concludes that entosis may contribute to aggressive cancers’ development by favoring cells with low tension setpoints, promoting the creation of aneuploid cell lineages, and supporting cell lineages with large scavenged nutrient sources. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. © The Author(s) 2024.
Keywords: signal transduction; review; cancer growth; animal; animals; cell death; apoptosis; stress activated protein kinase; molecular dynamics; enzyme activity; physiology; oncogene; tumor suppressor gene; enzyme regulation; cell migration; rhoa guanine nucleotide binding protein; cell adhesion; myosin adenosine triphosphatase; synaptophysin; hydroxymethylglutaryl coenzyme a reductase kinase; entosis; cellular stress signal; humans; human; actomyosin contractility
Journal Title: Experimental and Molecular Medicine
Volume: 56
Issue: 4
ISSN: 1226-3613
Publisher: Springer Nature  
Date Published: 2024-04-01
Start Page: 870
End Page: 876
Language: English
DOI: 10.1038/s12276-024-01227-w
PUBMED: 38565900
PROVIDER: scopus
PMCID: PMC11059358
DOI/URL:
Notes: Review -- Source: Scopus
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