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The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression
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Cellular senescence is a tumor-suppressive mechanism that permanently arrests cells at risk for malignant transformation. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.
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In the citing paper
“In 30–70% of senescent cells, this SASP entails pro-inflammatory, proapoptotic and pro-fibrotic factors7,31,40,59–64, some of which can cause previously non-senescent cells to become senescent both locally and at a distance in an endocrine manner24,39,47.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [60]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The secretion of these and similar proteins by senescent cells is predicted to cause chronic inflammation, at least locally and possibly systemically (91–93, 107).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [92]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Finally, the SASP also includes proteins that can help senescent cells evade immune recognition and clearance (92, 93).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [92]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“we observed an elevation of SA-β-gal activity, an increase in classical markers of cellular senescence (including p21/CDKN1A, GDF15 and IL8 mRNAs) and a reduction in LMNB1 mRNA, all consistent with a senescent phenotype”
From Single-cell and spatial transcriptomics map senescent vascular cells in arterial remodeling during atherosclerosis in mice (2025) · cites this paper as [32]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Further, the SASP can recruit immature immune-suppressive myeloid cells to prostate and liver tumors (Di Mitri et al., 2014; Eggert et al., 2016) and stimulate tumorigenesis by driving angiogenesis and metastasis (Coppe ´ et al., 2010).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Coppe et al., 2010
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“we generated a gene set (SenMayo) consisting of 125 previously identified senescence/SASP-associated factors”
From A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues (2022) · cites this paper as [81]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“factors secreted by senescent cells may directly or indirectly promote chronic inflammation that is thought to be a major factor in many, if not all, age-related diseases (2, 9, 10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [9]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Furthermore, senescent cells secrete bioactive mediators, including degradative enzymes, inflammatory cytokines and growth factors, which may further drive stem cell dysfunction with aging127.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [127]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“SASP contributes to local and systemic low-grade inflammation during aging, to age-related degenerative phenotypes, and to impairment of physical function.5,6,43”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“increased mitochondrial load/dysfunction and reactive oxygen species”
From Evolution of the immune system in humans from infancy to old age (2015) · cites this paper as [99]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The SASP is composed of pro-inflammatory cytokines, chemokines, exosomes, growth factors, and extracellular matrix-degrading proteins that are released into the surrounding tissue environment following the induction of growth arrest.24,25,26,27,28,29”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [24]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The SASP has also been shown to have paracrine activities, inducing senescence in nearby cells.24”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [24]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Control of the secretome in senescent cells is achieved at many levels, from transcriptional regulation to autocrine feedback loops, but persistent DDR appears to be critical for regulation of the SASP (Coppé et al. 2010).”
From Cellular senescence and its effector programs (2014) · cites this paper as Coppé et al. 2010
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Thus, the development of the SASP is largely dependent on a persistent DDR associated with senescence stimuli (Coppé et al. 2010).”
From Cellular senescence and its effector programs (2014) · cites this paper as Coppé et al. 2010
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The SASP of senescent cells is not static; it can change over time78–80 and varies depending on the type of cells that became senescent and how senescence was induced16,44,59,60,81.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [60]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“many SASP components directly or indirectly promote inflammation (59, 92, 93, 107, 108).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [92]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Sncs are often metabolically very active with a robust secretome [senescence-associated secretory phenotype (SASP)] (7).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells secrete a plethora of factors, including pro-inflammatory cytokines and chemokines, growth modulators, angiogenic factors, and matrix metalloproteinases (MMPs), collectively termed the senescent associated secretory phenotype (SASP) or senescence messaging secretome (SMS) (Figure 1; Table 2) (Coppe ´ et al., 2010; Kuilman and Peeper, 2009).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Coppe et al., 2010
The cited source says what the claim attributes to it.
In the citing paper
“For example, the SASP reinforces and spreads senescence in autocrine and paracrine fashions (Acosta et al., 2013; Coppe ´ et al., 2010; Kuilman and Peeper, 2009) and activates immune responses that eliminate senescent cells (Krizhanovsky et al., 2008a; Mun ˜ oz-Espı ´n and Serrano, 2014).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Coppe et al., 2010
The cited source says what the claim attributes to it.
In the citing paper
“Although cellular senescence can serve as a tumorigenic restrictive mechanism, it can also promote tumor growth and tumor invasiveness, through SASP-mediated regulatory effects”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [105]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent T cells are prevalent among Tem cells, and adopt a pro-inflammatory profile, similarly to the senescence-associated secreting phenotype (SASP) that was observed in fibroblasts [340].”
From Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition) (2021) · cites this paper as [340]
The cited source says what the claim attributes to it.
In the citing paper
“The SASP can also induce epithelial-to-mesenchymal transition (EMT) and increase tumor vascularization, suggesting that it has mostly protumorigenic properties (Coppé et al. 2010).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Coppé et al. 2010
The cited source says what the claim attributes to it.
In the citing paper
“To add extra confusion, the SASP can also differ based on cell type, cause of senescence, or even stage of senescence [37,95].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [95]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells contribute to aging and age-related pathologies21,22,23 through their senescence-associated secretory phenotype (SASP).24,25,26”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [24]
In the citing paper
“recent evidence suggests that senescent cells can morph their phenotype to SASP, which can paradoxically cause tumor growth (Coppé et al. 2010).”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Coppé et al. 2010
In the citing paper
“Although senescence acts as a protective mechanism against malignancies, serving as a tumor-suppressive mechanism”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Coppé et al. 2010
In the citing paper
“these factors promote shedding of membrane-associated proteins, degradation of signaling molecules, and/or ECM processing, thereby disrupting normal tissue framework and function”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [72]
In the citing paper
“senescent cells display extensive changes in gene expression, including the expression and secretion of many proinflammatory cytokines, chemokines, growth factors, and proteases; collectively these features are termed the senescence-associated secretory phenotype (SASP) (2, 7–10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [9]
In the citing paper
“Senescence-associated secretory phenotype (SASP) converts senescent cells into continuous sources of pro-inflammatory mediators, reactive oxygen species and metalloproteinases [43].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [43]
In the citing paper
“SASP consists of chemokines, cytokines, growth factors and metaloproteinases [43].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [43]
In the citing paper
“The SCI state in older individuals is thought to be caused in part by a complex process called cellular senescence, which is characterized by an arrest of cell proliferation and the development of a multifaceted senescence-associated secretory phenotype (SASP)53.”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [53]
In the citing paper
“Consistent SASP elements in the majority of senescent cells are IL-1α, IL-1β, IL-6, IL-8, IL-18, and TNF-α,15,105,110 all of which are clinically validated CVD risk factors.1,5”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [105]
In the citing paper
“sen(IR)-fibroblasts had increased expression of Csf1 transcripts (Extended Data Fig. 5e) and other growth factors40, which we confirmed were significantly increased at the protein level by proteomic analysis of the conditioned medium (Extended Data Fig. 5g).”
From Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages (2020) · cites this paper as [40]
In the citing paper
“We found that IP injections of PZ significantly decreased splenic expression of several SC biomarkers40,41, including Cdkn2a (p16), Cdkn1a (p21), and the SASP factors Il6, Cxcl12, Mmp3, and Tnfsf11 (Rankl) mRNA (Fig. 3e–j), indicating that PZ can effectively clear SCs in naturally aged mice.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [41]
In the citing paper
“Most senescent cells develop altered secretory activities known as a senescence-associated secretory phenotype (SASP) 77,78 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [77]
In the citing paper
“Furthermore, senescent cells secrete bioactive mediators, including degradative enzymes, inflammatory cytokines and growth factors, which may further drive stem cell dysfunction with aging127.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [127]
In the citing paper
“Accumulation of senescent cells in aging tissues can be another driver of chronic inflammation, as these cells secrete inflammatory factors, growth regulators, proteases and other signaling molecules127, affecting neighboring cells in the local environment and promoting senescence and inflammation.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [127]
In the citing paper
“senescent cells actively communicate with neighbouring cells and the extracellular matrix through a plethora of secretory factors, including extracellular proteases, cytokines and chemokines, and growth factors.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [90]
In the citing paper
“Components of the SASP have been shown to act in a paracrine manner, inducing senescence in surrounding cells, and this is thought to be a mechanism by which senescent cells contribute to age-related tissue dysfunction (Acosta et al., 2013; Baker et al., 2016; Coppé et al., 2010; Nelson et al., 2012).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Coppé et al., 2010
In the citing paper
“An unexpected property of senescent fibroblasts was their ability to secrete a wide array of proinflammatory cytokines including IL-6 and IL-1 and also other biological mediators such as matrix metalloproteinases [41].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [41]
In the citing paper
“This is known as the senescence associated secretory phenotype or SASP and is considered to be important for remodelling of ageing tissues [41, 42].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [41]
In the citing paper
“Other senescence markers previously used with other cell types, including formation of HP1-γ foci (28,29), spontaneous induction of γ-H2AX foci (30), and mRNA expression of SASP factors, such as IL6, IL8, CXCR1, and CXCR2 (8), were also increased in the CD28 -CD57 + subset”
From p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes (2013) · cites this paper as [8]
In the citing paper
“In particular, an increase in the basal production of proinflammatory cytokines, observed in different cell types, could be a major contributor to the age-related increase of the levels of such molecules observed in several cohorts of elderly subjects [19, 67, 68].”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [19]
In the citing paper
“Although the SASP is a feature shared by different senescence types, its regulation is considerably heterogeneous and is influenced by the cell type and the level and exposure duration to the initial senescence inducer [149].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [149]
In the citing paper
“Indeed, some types of cellular senescence, including the telomere-induced replicative type, are associated with an in vitro senescence-associated secretory phenotype (SASP), where cytokines and proteases are detected in culture media120.”
From The telomere syndromes (2012) · cites this paper as [120]
In the citing paper
“In addition, senescent cells express the cell cycle inhibitor p16INK4A (p16), senescence-associated β-galatosidase (SA-βgal), and an altered expression profile known as the senescence-associated secretory phenotype (SASP)11.”
From Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis (2016) · cites this paper as [11]
In the citing paper
“p27-induced senescence, which induces a SASP reminiscent of that observed in fibroblasts undergoing chronologic aging11.”
From Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis (2016) · cites this paper as [11]
In the citing paper
“The mechanisms responsible for the paradoxical role that senescence plays in tumorigenesis have remained obscure but are likely to lie in the senescent secretory profile that is defined by the cell of origin11.”
From Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis (2016) · cites this paper as [11]
In the citing paper
“On the other hand, the SASP can create a pro-tumorigenic environment (Coppe et al., 2010; Krtolica et al., 2001; Ruhland et al., 2016).”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Coppe et al., 2010
In the citing paper
“Metformin has also been reported to offset the effects of aging in the elderly and in cardiovascular disease (194, 198–200).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [194]
In the citing paper
“Several other studies using a variety of different cell types have reported that metformin inhibits NF-κB activation, decreases the production of inflammatory cytokines and the genes that code for the inflammatory response thus supporting the healthspan benefits of metformin (105, 194–196).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [194]
In the citing paper
“Senescent cells secrete a range of interleukins, inflammatory cytokines and growth factors (collectively referred to as SASP) that can affect surrounding cells (35).”
From Senolytic Combination of Dasatinib and Quercetin Alleviates Intestinal Senescence and Inflammation and Modulates the Gut Microbiome in Aged Mice (2021) · cites this paper as [35]
In the citing paper
“They have a distinctive phenotype, characterized by profound chromatin alterations and the development of a senescence-associated secretory phenotype (SASP), mainly comprised of cytokines, chemokines, matrix remodeling proteins, and growth factors, that has deleterious effects on tissue function, both locally and systemically”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Coppé et al., 2010
In the citing paper
“Cellular senescence impairs the ability of tissue regeneration and drives chronic low-grade inflammation, which exacerbates the aging process.5,6”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [5]
In the citing paper
“Cellular senescence impairs the ability of tissue regeneration and drives chronic low-grade inflammation, which exacerbates the aging process.5,6”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [5]
In the citing paper
“Cells present in the tumour microenvironment, such as fibroblasts, can become senescent and promote the growth and proliferation of tumour cells.7,39,40”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“There is mounting evidence that dysregulation or inappropriate activation of senescence contributes to tumour progression and malignancy.5,7,17”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“Senescent cells can contribute to the acquisition of invasive and metastatic properties of cancer cells, as well as the induction of tumour-associated angiogenesis.7,39”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“In this regard, the SASP has been shown to promote inflammation.7,72”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“telomere attrition accompanying each round of proliferation, leading to arrested cell division or ‘replicative senescence’”
From Evolution of the immune system in humans from infancy to old age (2015) · cites this paper as [99]
In the citing paper
“A third more recent addition to these fundamental changes of aged cells is the acquisition of the SASP, contributing to increased pro-inflammatory cytokine secretion and low-grade inflammation [99].”
From Evolution of the immune system in humans from infancy to old age (2015) · cites this paper as [99]
In the citing paper
“In elderly patients, a systemic abundance of proinflammatory cytokines (IL-1, TNF, and IL-6) can be detected, which is called senescence-associated secretory phenotype (SASP).45”
From Inflammatory bone marrow microenvironment (2019) · cites this paper as [45]
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“In addition, the SASP of SNCs will produce a large number of chemokines and will maintain the local inflammatory environment [40], which in turn is conducive for NK cell migration to SNCs and the production of cytotoxic effects against SNCs.”
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“Hundreds of SASP have been reported, among which the most common of factors include interleukin IL-1a, IL-6, and IL-1, and others such as IFN-γ, VEGF, ICAM-1, and GM-CSF [10, 13, 14], and some are released in the form of the exosome [14, 15].”
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HMGB2 holds the key to the senescence-associated secretory phenotype
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“24,30 The SASP has also been shown to have paracrine activities, inducing senescence in nearby cells.”
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Metadata
- Authors
- Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J.
- Affiliations
- Lawrence Berkeley National Laboratory (US)
- Buck Institute for Research on Aging (US)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2010-01-01
- Volume
- 5
- Issue
- 1
- Pages
- 99-118
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- PMC
- PMC4166495
- OpenAlex
- W2115852450
- Cited by
- 5,206
- References
- 150
- Citations by year
- 2026: 512 · 2025: 540 · 2024: 558 · 2023: 555 · 2022: 560 · 2021: 512 · 2020: 451 · 2019: 317 · 2018: 293 · 2017: 220 · 2016: 178 · 2015: 151 · 2014: 120 · 2013: 87 · 2012: 69
- FWCI
- 7.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R37AG009909, P01AG041122, P01AG017242)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- senescence-associated secretory phenotype, cellular senescence, tumor suppression, senescent fibroblasts, tumor microenvironment, inflammation, tumor progression, malignant transformation
- MeSH terms
- Cell Transformation, Neoplastic, Fibroblasts, Humans, Neoplasms, Phenotype, Cellular Senescence, Tumor Suppressor Proteins
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