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Updated: Apr 19, 2026
Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Tumour suppressors and cellular senescence
Adelyne S L Chan1, Sophia N Mowla, Parineeta Arora
1Department of Neurodegenerative Disease and MRC Prion Unit, UCL Institute of Neurology, Queen Square, London, WC1N 3BG.
Abstract:
Cellular senescence is a stable cell cycle arrest that normal cells undergo in response to a variety of intrinsic and extrinsic stimuli, including progressive telomere shortening, changes in telomeric structure or other forms of genotoxic as well nongenotoxic stress. Senescence is thought to have originated as a remodelling program that is active in embryonic development and acts as a key tumour suppressor mechanism during the reproductive stage in early adult life, by leading to the removal of potentially cancerous cells. However, in later adult life, it promotes organismal aging by compromising tissue repair and regeneration due to the accumulation of senescent cells, depletion of stem/progenitor cells and secretion of an array of inflammatory cytokines, chemokines and matrix metalloproteases. Whilst suppressing tumour formation in the senescent cells, these inflammatory cytokines, chemokines and metalloproteases can promote tumour progression and metastasis in the neighbouring cells. Herein, we review the molecular pathways that underlie cellular senescence and how it contributes towards tumour suppression.
Insights
Cellular senescence, a cell cycle arrest, acts as a tumor suppressor early in life but drives aging later by promoting inflammation and hindering tissue repair. This review explores senescence
Area of Science:
- Gerontology
- Molecular Biology
- Oncology
Background:
- Cellular senescence is a state of stable cell cycle arrest triggered by various cellular stresses.
- Initially, senescence functions as a tumor suppressor by eliminating potentially cancerous cells during early adult life.
- However, in later life, senescent cell accumulation impairs tissue repair and regeneration, contributing to organismal aging.
Purpose of the Study:
- To review the molecular pathways underlying cellular senescence.
- To elucidate the dual role of senescence in tumor suppression and aging.
- To discuss how senescence impacts tissue homeostasis and disease progression.
Main Methods:
- Literature review of molecular pathways involved in cellular senescence.
- Analysis of the role of senescence in embryonic development and early adult life.
- Examination of the contribution of senescent cells to aging and age-related diseases.
Main Results:
- Senescence is initiated by stimuli like telomere shortening and genotoxic stress.
- Senescence acts as a tumor suppressor by removing pre-cancerous cells.
- Accumulation of senescent cells promotes aging through inflammation and impaired regeneration.
Conclusions:
- Cellular senescence has a context-dependent role, acting as a tumor suppressor early in life and a driver of aging later.
- The senescence-associated secretory phenotype (SASP) contributes to both tumor suppression and promotion, as well as aging.
- Understanding senescence pathways is crucial for developing therapeutic strategies targeting aging and cancer.
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