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• W2855985248 abstract "Oncogene-induced senescence is a potent tumor-suppressive response. Paradoxically, senescence also induces an inflammatory secretome that promotes carcinogenesis and age-related pathologies. Consequently, the senescence-associated secretory phenotype (SASP) is a potential therapeutic target. Here, we describe an RNAi screen for SASP regulators. We identified 50 druggable targets whose knockdown suppresses the inflammatory secretome and differentially affects other SASP components. Among the screen candidates was PTBP1. PTBP1 regulates the alternative splicing of genes involved in intracellular trafficking, such as EXOC7, to control the SASP. Inhibition of PTBP1 prevents the pro-tumorigenic effects of the SASP and impairs immune surveillance without increasing the risk of tumorigenesis. In conclusion, our study identifies SASP inhibition as a powerful and safe therapy against inflammation-driven cancer." @default.
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• W2855985248 date "2018-07-01" @default.
• W2855985248 modified "2023-10-17" @default.
• W2855985248 title "PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells" @default.
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• W2855985248 doi "https://doi.org/10.1016/j.ccell.2018.06.007" @default.
• W2855985248 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6048363" @default.
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