Journal
ISCIENCE
Volume 24, Issue 8, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2021.102902
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Funding
- National Cancer Institute [RO1CA154649]
- American Association for Cancer Research/Stand Up To Cancer [SU2C-AACR-IRG-01-16]
- American Association for Cancer Research, the scientific partner of SU2C
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Research has identified JNK and p38 stress-activated kinase signaling as an inducer of cell entosis in response to UV radiation. Cells with high stress signaling levels are ingested and killed by those with low levels, while also triggering apoptosis and necrosis responses in stressed cells. These findings demonstrate the cross talk between different forms of cell death that can occur simultaneously in response to UV radiation.
Entosis is a cell death mechanism that is executed through neighbor cell ingestion and killing that occurs in cancer tissues and during development. Here, we identify JNK and p38 stress-activated kinase signaling as an inducer of entosis in cells exposed to ultraviolet (UV) radiation. Cells with high levels of stress signaling are ingested and killed by those with low levels, a result of heterogeneity arising within cell populations over time. In stressed cells, entosis occurs as part of mixed-cell death response with parallel induction of apoptosis and necrosis, and we find that inhibition of one form of cell death leads to increased rates of another. Together, these findings identify stress-activated kinase signaling as a new inducer of entosis and demonstrate cross talk between different forms of cell death that can occur in parallel in response to UV radiation.
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