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Updated: Nov 19, 2025
Simultaneous Imaging and Flow-Cytometry-based Detection of Multiple Fluorescent Senescence Markers in Therapy-Induced Senescent Cancer Cells
Published on: July 12, 2022
Cancer Response to Therapy-Induced Senescence: A Matter of Dose and Timing
Maria Patrizia Mongiardi1, Manuela Pellegrini1, Roberto Pallini2
1CNR-Institute of Biochemistry and Cell Biology, Campus Adriano Buzzati Traverso, Via Ercole Ramarini 32, Monterotondo Scalo, 00015 Rome, Italy.
Abstract:
Cellular senescence participates to fundamental processes like tissue remodeling in embryo development, wound healing and inhibition of preneoplastic cell growth. Most senescent cells display common hallmarks, among which the most characteristic is a permanent (or long lasting) arrest of cell division. However, upon senescence, different cell types acquire distinct phenotypes, which also depend on the specific inducing stimuli. Senescent cells are metabolically active and secrete a collection of growth factors, cytokines, proteases, and matrix-remodeling proteins collectively defined as senescence-associated secretory phenotype, SASP. Through SASP, senescent cells modify their microenvironment and engage in a dynamic dialog with neighbor cells. Senescence of neoplastic cells, at least temporarily, reduces tumor expansion, but SASP of senescent cancer cells as well as SASP of senescent stromal cells in the tumor microenvironment may promote the growth of more aggressive cancer subclones. Here, we will review recent data on the mechanisms and the consequences of cancer-therapy induced senescence, enlightening the potentiality and the risk of senescence inducing treatments.
Insights
Cellular senescence, a state of permanent cell division arrest, plays roles in development and wound healing. However, its role in cancer is complex, as senescence-associated secretory phenotype (SASP) can promote tumor growth.
Area of Science:
- Cellular and Molecular Biology
- Oncology
- Aging Research
Background:
- Cellular senescence is a fundamental biological process involved in development, wound healing, and tumor suppression.
- Senescent cells exhibit a permanent cell division arrest and a distinct senescence-associated secretory phenotype (SASP).
- SASP involves the secretion of various factors that modify the cellular microenvironment and influence neighboring cells.
Purpose of the Study:
- To review recent data on the mechanisms and consequences of cancer-therapy induced senescence.
- To explore the dual role of senescence in cancer, including its potential to inhibit tumor growth and promote aggressive subclones.
- To discuss the therapeutic potential and risks associated with senescence-inducing treatments.
Main Methods:
- Literature review of recent data on cancer-therapy induced senescence.
- Analysis of the mechanisms underlying cellular senescence and SASP.
- Evaluation of the impact of SASP in the tumor microenvironment.
Main Results:
- Senescence is a complex process with context-dependent outcomes in cancer.
- Senescent cancer cells and stromal cells within the tumor microenvironment can secrete SASP.
- SASP can paradoxically promote the growth of more aggressive cancer subclones.
Conclusions:
- Cancer-therapy induced senescence presents both opportunities and risks for cancer treatment.
- Understanding the intricate mechanisms of senescence and SASP is crucial for developing effective therapeutic strategies.
- Targeting senescence pathways requires careful consideration of their multifaceted roles in cancer progression.
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