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
PubMed

Insights

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.