ArticleGenes & development2011
Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 642 papers, 1 of them a synthesis that pooled it.
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Who cites it
642 citing papers in PubMed, 1 synthesis or guideline pooled it, 968 citations in OpenAlex.
- Cross-Trait Meta-Analysis Reveals a Genetic Link between Inflammation and Aging in Giant Cell Arteritis.Aging and disease · 2025Pooled it
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- Cellular senescence and the SASP in skeletal ageing: convergent mechanisms of progressive bone loss in osteoporosis.Biogerontology · 2026Review
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- Disruption of CDK4/6-RARα-NF-κB axis attenuates senescence-associated inflammation and improves function during aging and following chemotherapy.Nature aging · 2026Article
- CDK4/6 inhibition induces a senescence-associated secretory phenotype via delayed NF-κB activation.Life science alliance · 2026Article
- Berberine and its derivatives as candidate modulators of immunosenescence: a critical evaluation.Biogerontology · 2026Review
- Inhibiting cyclin D1-CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline.Nature aging · 2026Article
- Mechanisms and therapeutic potential of therapy-induced cellular senescence in radiotherapy- and chemotherapy-related alimentary tract mucositis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Review
- Inflammation-linked aging signals in frozen single-cell foundation models: donor-aware detection and robustness testing.Biogerontology · 2026Article
- Royal jelly suppresses senescence-associated secretory phenotype in senescent human epidermal keratinocytes.Molecular biology reports · 2026Article
- Therapy-induced senescence rewires the melanoma secretome to promote antitumor immune response and augment cell therapies.Journal for immunotherapy of cancer · 2026Article
- Review
- Inhibition of inflammation and senescence with azole compound C7 enables expansion of hematopoietic stem and progenitor cells.Stem cells translational medicine · 2026Article
- Review
- Aberrant immunomodulatory signature in β-propeller protein-associated neurodegeneration patient iPSC-derived microglia.Scientific reports · 2026Article
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Methyl Caffeate Binds to IQGAP1 and Inhibits the Senescence-Associated Secretory Phenotype in Senescent Cells.International journal of molecular sciences · 2026Article
- NF-κB-activated fibroblasts orchestrate inflammaging and emergence of pro-inflammatory granzyme KImmunity · 2026Article
- Protein phosphatase 2 phosphatase activator (PTPA) promotes oncogene-induced senescence and carboplatin response in human malignant pleural mesothelioma cells.Cellular oncology (Dordrecht, Netherlands) · 2026Article
582 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.