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Updated: Feb 24, 2026

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
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Spatial and Temporal Control of Senescence.

Yoko Ito1, Matthew Hoare2, Masashi Narita1

  • 1Cancer Research UK Cambridge Centre, Li Ka Shing Centre, University of Cambridge, Cambridge, CB2 0RE, UK.

Trends in Cell Biology
|August 21, 2017
PubMed
Summary

Cellular senescence, a tumor suppressor mechanism, involves cells secreting factors via the senescence-associated secretory phenotype (SASP). NOTCH signaling dynamically regulates SASP composition, influencing its beneficial or detrimental effects.

Keywords:
C/EBPβNOTCHinflammationlateral inductionsenescencesenescence-associated secretory phenotype (SASP)

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Area of Science:

  • Cellular Biology
  • Oncology
  • Molecular Signaling

Background:

  • Cellular senescence acts as a tumor suppressor, inducing stable cell cycle arrest.
  • Senescent cells release various factors through the senescence-associated secretory phenotype (SASP).
  • SASP composition is increasingly recognized as dynamic and spatially regulated.

Purpose of the Study:

  • To review the current understanding of temporal and spatial regulation of the SASP.
  • To highlight the role of NOTCH signaling in modulating SASP composition.

Main Methods:

  • Review of existing literature on cellular senescence and SASP regulation.
  • Discussion of findings related to the dynamic and spatial control of SASP.
  • Focus on the impact of NOTCH signaling pathways.

Main Results:

  • The composition of the SASP is not static but changes over time and space.
  • These compositional changes dictate whether the senescence program is beneficial (e.g., pro-inflammatory) or detrimental (e.g., immunosuppressive).
  • NOTCH signaling has been identified as a key regulator of SASP composition.

Conclusions:

  • Understanding the dynamic regulation of SASP is crucial for deciphering its dual roles in health and disease.
  • NOTCH signaling represents a significant pathway influencing SASP output and its functional consequences.
  • Targeting NOTCH signaling could offer therapeutic strategies to modulate senescence-associated outcomes.