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• W2061765285 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." @default.
• W2061765285 created "2016-06-24" @default.
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• W2061765285 date "2011-10-06" @default.
• W2061765285 modified "2023-10-16" @default.
• W2061765285 title "Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity" @default.
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• W2061765285 doi "https://doi.org/10.1101/gad.17276711" @default.
• W2061765285 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3205583" @default.
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