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Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion
Open accessAbstract
Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells. Paradoxically, senescent cells also secrete factors that alter tissue microenvironments. The pathways regulating this secretion are unknown. We show that damaged human cells develop persistent chromatin lesions bearing hallmarks of DNA double-strand breaks (DSBs), which initiate increased secretion of inflammatory cytokines such as interleukin-6 (IL-6). Cytokine secretion occurred only after establishment of persistent DNA damage signalling, usually associated with senescence, not after transient DNA damage responses (DDRs). Initiation and maintenance of this cytokine response required the DDR proteins ATM, NBS1 and CHK2, but not the cell-cycle arrest enforcers p53 and pRb. ATM was also essential for IL-6 secretion during oncogene-induced senescence and by damaged cells that bypass senescence. Furthermore, DDR activity and IL-6 were elevated in human cancers, and ATM-depletion suppressed the ability of senescent cells to stimulate IL-6-dependent cancer cell invasiveness. Thus, in addition to orchestrating cell-cycle checkpoints and DNA repair, a new and important role of the DDR is to allow damaged cells to communicate their compromised state to the surrounding tissue.
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In the citing paper
“Many such stressors activate DNA damage response signaling and activation of the p53/p21CIP1/WAF1, p16INK4a/retinoblastoma protein or other pathways, resulting in cell cycle arrest and the development of a senescence-associated secretory phenotype (SASP)24,40,48−53”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [50]
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
“Nevertheless, there is substantial overlap among SASPs; proinflammatory cytokines are the most highly conserved feature, cutting across many different cell types and senescence-inducing stimuli (33, 42, 96, 99, 100, 112–114).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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 primarily a property of cells that senesce owing to, or accompanied by, genomic damage or epigenomic perturbation.”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“These nuclear structures contain the activated DDR proteins that ensure the persistent DDR signaling (43) that is needed for both the senescence growth arrest and the SASP (32, 42, 43).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“Of particular importance, these DDR proteins stimulate the SASP only after persistent DDR signaling has been established.”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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“Furthermore, p53 inactivation in cells that do not express p16INK4a, which renders the senescence growth arrest irreversible (10), causes cells to resume proliferation, but the SASP remains active (32, 42).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“That is, the rapid robust DDR that occurs immediately after DNA damage does not induce a SASP; rather, the SASP develops slowly—over several days in culture—and only after the initial DDR subsides (32, 42).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“Many, but not all, SASP components are positively regulated by the DDR proteins ATM, NBS1 (Nijmegen breakage syndrome 1), and CHK2 (checkpoint kinase 2) (42, 67).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“In contrast, cells that senesce owing to DNA damage, dysfunctional telomeres, epigenomic disruption, mitogenic signals, oxidative stress, and other senescence-inducing stimuli develop a SASP of varying qualities and robustness (32, 33, 42, 67, 94, 96, 99, 100, 112–114).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“ATM, NBS1 and CHK2 prime SASP genes for activation, as depletion of these DDR upstream regulators dampens cytokine production in response to genotoxic stress86”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [86]
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
“Because p53 also limits SASP gene expression (Coppé et al., 2008; Rodier et al., 2009), we depleted p53 in WT and rho0 cells and measured IL1A and IL1B mRNA levels.”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Rodier et al., 2009
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In the citing paper
“IR robustly activates p53, which subsides to a low chronic level in 7–10 days as the SASP develops (Coppé et al., 2008; Rodier et al., 2009).”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Rodier et al., 2009
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
“A signature pro-inflammatory secretory phenotype takes 7–10 days to develop under DDR (Coppe et al, 2008; Rodier et al, 2009).”
From Feedback between p21 and reactive oxygen production is necessary for cell senescence (2010) · cites this paper as Rodier et al, 2009
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
“Own (Supplementary Figure S1A) and published (Coppe et al, 2008; Rodier et al, 2009) data indicated that a full senescent phenotype develops over 7–10 days in human fibroblasts.”
From Feedback between p21 and reactive oxygen production is necessary for cell senescence (2010) · cites this paper as Rodier et al, 2009
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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 [27]
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
“In addition, expression of the CDK inhibitors p16 or p21 leads to the induction of senescence without the development of a DDR; this senescent phenotype lacks a proinflammatory SASP (Rodier et al. 2009).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
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
“Loss of ataxia telangiectasia-mutated (ATM) or other factors responding to DNA damage (such as NBS1 and CHK2) leads to reductions in some SASP factors, such as IL6 and IL8, central components of SASP, during not only DDR-induced senescence but also OIS (Rodier et al. 2009).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
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
“Induction of p21 and a Notch- driven SASP are considered early events 70,75,76 , whereas upregulation of p16 INK4a and an NF- κB- driven SASP are evident at later stages of senescence 71,77,78 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [78]
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
“Alkylating agents 27,95,96 (for example, cisplatin, cyclophosphamide and temozolomide), topoisomerase inhibitors 27,65,91,95 (such as doxorubicin, etoposide and camptothecin) and γ- irradiation 78 , but also microtubule inhibitors 27,97,98 (for example, paclitaxel) and, to a lesser extent, vinca alkaloids 78 (for example, vincristine), have all been identified as senescence inducers in preclinical”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [78]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In contrast to positive regulation by the DDR, p53 negatively regulates or, more accurately, restrains the SASP (32, 42) (Figure 2).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
The cited source says what the claim attributes to it.
In the citing paper
“SASP is both promoted by DDR13 and can promote DDR and TAF formation in an autocrine and paracrine fashion14–16.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“Inhibition of p53 has the opposite effect, as it further enhances SASP following a senescence-inducing insult86, which may contribute to the generation of an inflammatory microenvironment that favours senescence escape and malignant transformation”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [86]
The cited source says what the claim attributes to it.
In the citing paper
“persistent DDR signalling is often required to initiate inflammatory cytokine secretion86”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [86]
The cited source says what the claim attributes to it.
In the citing paper
“Persistent DDR activity is required for the induction of several proinflammatory SASP factors, such as IL-6 and IL-8 (Rodier et al. 2009).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Rodier et al. 2009
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, dysfunctional mitochondria,195 persistent DNA damage response,196 CCAAT/enhancer-binding protein β (C/EBPβ) and NF-κB,197 mTOR, and other factors are involved in regulating SASP.194”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [196]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells induced by either genotoxic stress, replicative exhaustion, or oncogenic stress secrete myriad factors associated with inflammation, proliferation, and modulation of the extracellular matrix (ECM) (Acosta et al. 2008; Kuilman et al. 2008; Rodier et al. 2009).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
The cited source says what the claim attributes to it.
In the citing paper
“Of note, DDR-independent senescence has also been reported in some experimental conditions where p16, p38MAPK, or ATR is constitutively activated or tumor suppressor Pten is completely lost (Toledo et al. 2008; Rodier et al. 2009; Alimonti et al. 2010; Freund et al. 2011).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
In the citing paper
“Senescent cells remain viable, have alterations in metabolic activity and undergo dramatic changes in gene expression and develop a complex senescence-associated secretory phenotype.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Rodier et al., 2009
In the citing paper
“They undergo dramatic gene expression changes along with chromatin remodeling and engagement of a persistent DNA damage response (DDR) (Rodier et al., 2009; Wang et al., 2009; Sulli et al., 2012; Chandra et al., 2015).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Rodier et al., 2009
In the citing paper
“DNA damage, dysfunctional telomeres, genomic damage, epigenomic perturbation, mitogenic proliferative signals, oxidative stress or other senescence-inducing stimuli, all leading to prolonged DDR express SASP to different extents (Acosta et al., 2008; Kuilman et al., 2008; Rodier et al., 2009; Coppé et al., 2010b; Pazolli et al., 2012).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Rodier et al., 2009
In the citing paper
“In general terms, DNA damage activates DDR, a p53/21-dependent response that is originally transient but which can become persistent if the damage is severe enough, and which can also be reversed through the p16/pRB pathways [219], [241].”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [241]
In the citing paper
“the SASP does not depend on either p53 or p16INK4a, which suggests that it is controlled by an independent branch of the senescence regulatory network (2, 10, 20, 26).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [20]
In the citing paper
“However, senescent cells acquire a “senescence-associated secretory phenotype” (SASP), secreting many pro-inflammatory cytokines, proteases, and growth and angiogenesis factors that can disrupt microenvironments and compromise tissue structure and function thereby contributing to local and systemic ageing-associated pathologies47 and promote cancer64.”
From The central role of DNA damage in the ageing process (2021) · cites this paper as [47]
In the citing paper
“although cellular senescence in vitro may also occur without detectable DDR [31,32].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [32]
In the citing paper
“In addition, tumor cells activate the PKA-CREB and P38 pathways by producing cAMP, thereby causing DNA damage and senescence of T cells [51, 53, 58–63].”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [62]
In the citing paper
“Cell cycle controlling proteins p16, p21, and p53, normally inhibit cell cycle progression and have been shown to be accumulated in senescent cells [49–51].”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [50]
In the citing paper
“Cellular senescence is a primary aging process and tumor suppressive mechanism characterized by irreversible growth arrest, apoptosis resistance, production of a senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and alterations in DNA and chromatin.”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [22]
In the citing paper
“Hallmarks of the cellular senescence phenotype include irreversible growth arrest, a senescence-associated secretory phenotype (SASP) (Box 1), apoptosis resistance, mitochondrial dysfunction [21], persistent DNA damage foci [22] and epigenetic remodeling, which includes formation of senescence-associated heterochromatin foci [23].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [22]
In the citing paper
“The p53-dependence of CCL2 production may distinguish CCL2 from some of the other chemokines produced in senescent cells, which are dependent on the senescent state but are produced independently of p53 (Coppé et al., 2008; Rodier et al., 2009).”
From p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells (2013) · cites this paper as Rodier et al., 2009
In the citing paper
“Senescent cells secrete a distinct suite of inflammatory cytokines and chemokines depending upon whether senescence is induced by genotoxic stress, [23] or mitochondrial dysfunction, as in the form of deficiencies in mitochondrial sirtuins or damage to mitochondrial DNA [24]”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [23]
In the citing paper
“In addition to the downregulation of cell cycle genes, senescent cells are programmed to secrete different chemokines, pro-inflammatory cytokines, growth factors, and matrix-remodeling enzymes that define the SASP [136,147,148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“Activation of the SASP program requires a sustained DDR signal but is independent of p53, p21, and p16 (the mediators of cell cycle arrest in senescent cells) [147,148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“ATM signaling does not regulate the entire production of SASP factors, although it is required for the secretion of IL-6 and IL-8, the most conserved and robustly expressed inflammatory cytokines [148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“SASP factor production requires continuous DNA damage signaling [148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“the secretome of senescent tumor cells can also drive tumor progression by promoting inflammation and potentially stimulating the growth and invasiveness of nearby tumor cells [148,154,163].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“DNA damage is a potent activator of inflammatory signaling and senescence (Coppé et al, 2008; Rodier et al, 2009; Brzostek‐Racine et al, 2011; Härtlova et al, 2015).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Rodier et al, 2009
In the citing paper
“Initially, induction of persistent DDR signaling in cell cultures including fibroblasts (Coppé et al, 2008; Rodier et al, 2009), bone marrow‐derived macrophages (BMDMs) (Härtlova et al, 2015), and primary monocytes (Brzostek‐Racine et al, 2011) was found to elicit the SASP (Coppé et al, 2008).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Rodier et al, 2009
In the citing paper
“This secretory profile was found to be at least partially ATM‐dependent, implying the importance of DSB repair specifically in immune activation (Rodier et al, 2009; Brzostek‐Racine et al, 2011).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Rodier et al, 2009
In the citing paper
“These SASP factors are part of the IL-1-dependent inflammatory arm57, and are normally expressed by DNA damage-induced senescent cells.”
From Algorithmic assessment of cellular senescence in experimental and clinical specimens (2021) · cites this paper as [57]
In the citing paper
“These SASP factors are part of the IL-1-dependent inflammatory arm57, and are normally expressed by DNA damage-induced senescent cells.”
From Algorithmic assessment of cellular senescence in experimental and clinical specimens (2021) · cites this paper as [57]
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Citations
Cites
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Metadata
- Authors
- Rodier, F., Coppé, J.-P., Patil, C. K., Hoeijmakers, W. A. M., Muñoz, D. P., Raza, S. R., Freund, A., Campeau, E., Davalos, A. R., & Campisi, J.
- Affiliations
- Lawrence Berkeley National Laboratory (US)
- Buck Institute for Research on Aging (US)
- Corresponding author
- Campisi, Judith
- Venue
- Nature Cell Biology
- Published
- 2009-07-13
- Volume
- 11
- Issue
- 8
- Pages
- 973-979
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC2743561
- OpenAlex
- W2116054786
- Cited by
- 2,232
- References
- 31
- Citations by year
- 2026: 126 · 2025: 143 · 2024: 152 · 2023: 158 · 2022: 159 · 2021: 168 · 2020: 154 · 2019: 147 · 2018: 139 · 2017: 149 · 2016: 113 · 2015: 105 · 2014: 118 · 2013: 102 · 2012: 108
- FWCI
- 64.86
- Type
- journal article
- Language
- en
- Update notices
- erratum (2009-10-01)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG017242, P30AG025708, AG025708, P01AG017242)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- DNA damage response, senescence-associated secretory phenotype, IL-6 secretion, oncogene-induced senescence, ATM, NBS1, Chk2, DNA double-strand breaks, tumour invasiveness, senescence-associated inflammation, p53, retinoblastoma protein
- MeSH terms
- Cell Line, Cells, Cultured, DNA Damage, DNA-Binding Proteins, Enzyme-Linked Immunosorbent Assay, Fibroblasts, Humans, Male, Microscopy, Fluorescence, Nuclear Proteins, Transfection, Blotting, Western, Signal Transduction, Interleukin-6, Tumor Suppressor Protein p53, Cytokines, Telomere, Cellular Senescence, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Telomerase, Cyclin-Dependent Kinase Inhibitor p16, Tumor Suppressor Proteins, RNA, Small Interfering, Green Fluorescent Proteins, Ataxia Telangiectasia Mutated Proteins, Checkpoint Kinase 2
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