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Notch Signaling Mediates Secondary Senescence
Yee Voan Teo1, Nattaphong Rattanavirotkul2, Nelly Olova3
1Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02903, USA.
Cell Reports
|April 25, 2019
Summary
Oncogene-induced senescence (OIS) has two distinct cell types: primary (Ras-driven) and secondary (Notch-driven). Secondary OIS requires Notch signaling, not just SASP, and shows functional diversification.
Area of Science:
- Cellular senescence
- Cancer biology
- Tumor suppression
Background:
- Oncogene-induced senescence (OIS) is a tumor suppressive mechanism.
- Senescence can spread to neighboring cells via the senescence-associated secretory phenotype (SASP).
- Primary and secondary senescent cells are not currently viewed as functionally distinct.
Purpose of the Study:
- To investigate the functional and transcriptional differences between primary and secondary oncogene-induced senescence.
- To determine the role of Notch signaling and SASP in secondary senescence.
Main Methods:
- Single-cell transcriptional analysis
- In vitro and in vivo studies of oncogene-induced senescence
- Assessment of Notch signaling and SASP factors
Main Results:
- Two distinct transcriptional endpoints for OIS were identified: primary (Ras-driven) and secondary (Notch-driven).
- Secondary OIS requires Notch signaling, challenging the notion that SASP alone is sufficient.
- Notch signaling partially suppresses SASP in secondary senescent cells, which also exhibit increased fibrillar collagen production.
Conclusions:
- Primary and secondary senescent cells represent functionally distinct states.
- Notch signaling plays a critical, previously unrecognized role in secondary OIS.
- Functional diversification in senescence may involve distinct signaling pathways and molecular outputs.
Keywords:
CEBPBNotchTGFBbystander senescenceoncogene induced senescenceparacrine senescencesecondary senescencesenescencesenescence associated secretory phenotypesingle-cell RNA sequencingMore Related Videos
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