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Senescence Rewires Microenvironment Sensing to Facilitate Antitumor Immunity
Hsuan-An Chen1,2, Yu-Jui Ho1, Riccardo Mezzadra1
1Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York.
Cancer Discovery
|October 27, 2022
Summary
Cellular senescence enhances tumor cell visibility to the immune system by altering cell surface receptors and improving environmental sensing. This improves immune clearance of senescent cells, crucial for cancer rejection.
Area of Science:
- Immunology
- Cell Biology
- Oncology
Background:
- Cellular senescence is a state of stable cell-cycle arrest.
- Senescence is often accompanied by a secretory program that can aid immune clearance.
- Senescence can trigger CD8 T cell-mediated tumor rejection in liver cancer models.
Discussion:
- Senescence remodels the cell-surface proteome, altering how tumor cells sense environmental factors like type II interferon (IFNγ).
- Senescent cells upregulate the IFNγ receptor, becoming hypersensitive to IFNγ and enhancing antigen-presenting machinery.
- These changes are also observed in human tumor cells experiencing therapy-induced senescence.
Key Insights:
- Disrupting IFNγ sensing in senescent cells impairs their immune clearance without affecting the senescence state or secretory program.
- Senescent cells exhibit enhanced abilities in both sending and receiving environmental signals.
- Both signal sending and receiving are essential for effective immune surveillance of senescent cells.
Outlook:
- Senescence engages interplay between tissue remodeling and sensing programs to increase tumor cell visibility to the adaptive immune system.
- This facet of senescence establishes reciprocal signaling interactions that can be therapeutically induced to boost antitumor immunity.
- Further research can explore therapeutic strategies targeting these senescence-induced signaling pathways for cancer treatment.
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