The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity
Open accessAbstract
Cellular senescence acts as a potent barrier to tumorigenesis and contributes to the anti-tumor activity of certain chemotherapeutic agents. Senescent cells undergo a stable cell cycle arrest controlled by RB and p53 and, in addition, display a senescence-associated secretory phenotype (SASP) involving the production of factors that reinforce the senescence arrest, alter the microenvironment, and trigger immune surveillance of the senescent cells. Through a proteomics analysis of senescent chromatin, we identified the nuclear factor-κB (NF-κB) subunit p65 as a major transcription factor that accumulates on chromatin of senescent cells. We found that NF-κB acts as a master regulator of the SASP, influencing the expression of more genes than RB and p53 combined. In cultured fibroblasts, NF-κB suppression causes escape from immune recognition by natural killer (NK) cells and cooperates with p53 inactivation to bypass senescence. In a mouse lymphoma model, NF-κB inhibition bypasses treatment-induced senescence, producing drug resistance, early relapse, and reduced survival. Our results demonstrate that NF-κB controls both cell-autonomous and non-cell-autonomous aspects of the senescence program and identify a tumor-suppressive function of NF-κB that contributes to the outcome of cancer therapy.
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“First, the transcription factors nuclear factor κB (NF‐κB) and CCAAT/enhancer‐binding protein (C/EBP‐β) were identified as positive regulators of SASP factor expression.”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [49]
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.
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“Given the proinflammatory nature of the SASP, it is not surprising that senescent cells can attract immune cells, including destructive leukocytes of the innate and adaptive immune systems (131, 132, 135).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [135]
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.
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“The SASP cytokines that are responsible for these immune responses are incompletely understood but are very likely numerous (132, 135).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [135]
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.
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“Among the cells that participate in the clearance of senescent cells are natural killer cells, macrophages, and T cells (131, 135, 139).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [135]
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“The NF- κB, p38, mTOR and C/EBPβ signalling pathways are major components of the SASP 63-67 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [64]
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“In contrast, at least some SASP components can be chemosensitizing.”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [135]
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“For example, global suppression of the SASP (through NF-κB inhibition) promoted resistance to chemotherapy in a mouse lymphoma model (135).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [135]
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“In senescent fibroblasts and in oncogene-induced senescence, the SASP is closely controlled by signalling through NF-κB1617.”
From Chronic inflammation induces telomere dysfunction and accelerates ageing in mice (2014) · cites this paper as [16]
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“The results indicated that the DRISR closest to ATAC-UP regions were significantly enriched (q-value < 0.05) in 43 motifs (Fig. 2F), including NF-κB (35), Jun-AP1 (36), Batch2 (37), Stat3, HIF-1α, and CTCF (11, 21), which are known to be involved in cellular senescence or inflammatory SASP gene expression.”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [35]
In the citing paper
“Most of the cascades involved in inducing and dynamically regulating SASP ultimately converge on the activation of two transcription factors, NF-κB and CEBPβ which are found to be enriched in the chromatin fractions of senescent cells (Acosta et al., 2008; Kuilman et al., 2008; Chien et al., 2011; Ohanna et al., 2011; Huggins et al., 2013).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Chien et al., 2011
In the citing paper
“NF-κB has a crucial role in controlling the SASP (18, 19, 49) (Fig. 3D)”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [49]
In the citing paper
“Even more upstream, inhibition of nuclear factor κB (NF-κB) abrogated p53-mediated senescence.55”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [55]
In the citing paper
“Most SASP regulators converge to the CCAAT/enhancer-binding protein β (C/EBP-β) and nuclear factor kappa-B (NF-κB) transcription factors that cooperatively regulate SASP factors induction in various senescence contexts [153,154,155].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [155]
In the citing paper
“Considering the central role of NF-κB transcriptional activity in SASP induction, NF-κB inhibition in senescent cells selectively represses SASP genes that require this transcription factor [155].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [155]
In the citing paper
“As the p53 response efficiency declines during aging [228], aerobic glycolysis is increased as well as the proinflammatory SASP via NF-κB signaling [155].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [155]
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Metadata
- Authors
- Chien, Y., Scuoppo, C., Wang, X., Fang, X., Balgley, B., Bolden, J. E., Premsrirut, P., Luo, W., Chicas, A., Lee, C. S., Kogan, S. C., & Lowe, S. W.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Tsinghua University (CN)
- University of Maryland, College Park (US)
- University of California, San Francisco (US)
- Memorial Sloan Kettering Cancer Center (US)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2011-10-06
- Volume
- 25
- Issue
- 20
- Pages
- 2125-2136
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3205583
- OpenAlex
- W2061765285
- Semantic Scholar
- 6dc1897ec48a6521984255282828603c81174912
- Cited by
- 1,046
- References
- 58
- Citations by year
- 2026: 104 · 2025: 101 · 2024: 100 · 2023: 68 · 2022: 95 · 2021: 96 · 2020: 81 · 2019: 73 · 2018: 73 · 2017: 40 · 2016: 68 · 2015: 43 · 2014: 34 · 2013: 40 · 2012: 26
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (submittedVersion)
- Swinburne figshare (Swinburne University of Technology) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Leukemia and Lymphoma Society
- National Institutes of Health
- National Institute on Aging (R56AG016379, AG-16379, R01AG016379)
- National Cancer Institute (CA 122715, R42CA122715, R21CA143177, CA 143177, R41CA122715)
- National Institute of General Medical Sciences (T32GM008444)
- National Center for Research Resources (RR 021239, R44RR021239, R43RR021239)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, senescence-associated secretory phenotype, NF-κB, NF-κB p65, chemosensitivity, drug resistance, p53, Rb, natural killer cells, tumor suppression, lymphoma, senescence escape
- MeSH terms
- Animals, Cell Line, Cell Survival, Drug Resistance, Humans, Lymphoma, Phenotype, Protein Synthesis Inhibitors, Tetracycline, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Cellular Senescence, RNA, Small Interfering, Cell Line, Tumor, Mice, Transcription Factor RelA
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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