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Entosis is induced by ultraviolet radiation
Ruoyao Chen1,2, Abhineet Ram3, John G Albeck3
1Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Iscience
|August 17, 2021
Summary
Stress-activated kinase signaling, including JNK and p38, induces entosis, a cell death process. This occurs alongside apoptosis and necrosis, with cell death pathways influencing each other.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Entosis is a programmed cell death mechanism involving cell engulfment, observed in cancer and development.
- The precise triggers and regulation of entosis, particularly in response to environmental stressors, remain incompletely understood.
Purpose of the Study:
- To identify novel inducers of entosis in cells exposed to ultraviolet (UV) radiation.
- To investigate the relationship between entosis and other cell death pathways like apoptosis and necrosis.
Main Methods:
- Exposure of cells to ultraviolet (UV) radiation.
- Analysis of stress-activated kinase signaling pathways (JNK and p38).
- Observation and quantification of entosis, apoptosis, and necrosis rates.
- Pharmacological inhibition of specific cell death pathways.
Main Results:
- JNK and p38 stress-activated kinase signaling were identified as inducers of entosis upon UV exposure.
- Heterogeneity in stress signaling levels within cell populations led to the ingestion and death of highly stressed cells by less stressed neighbors.
- Entosis occurred concurrently with apoptosis and necrosis, forming a mixed-cell death response.
- Inhibition of one cell death pathway (e.g., apoptosis) resulted in increased rates of other pathways (e.g., necrosis or entosis).
Conclusions:
- Stress-activated kinase signaling (JNK/p38) is a newly identified inducer of entosis.
- Entosis is integrated into a broader, parallel cell death response to UV radiation, involving apoptosis and necrosis.
- There is significant cross-talk between distinct cell death mechanisms, where modulating one impacts the others.
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