Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor

By Jean-Philippe Coppé. 2009

632 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/87bb30c12ba3f01b408135f48d9115ff85a6c2ab

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Citations in the corpus

• Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “, 2001) or contributing to epithelial to mesenchymal transition (Coppé et al., 2008).”
• Cellular senescence promotes adverse effects of chemotherapy and cancer relapse (2016, methodology): “Senescence was further confirmed by elevated levels of mRNAs encoding p16INK4a and the SASP components IL-1α, IL-6, Mmp-3, Mmp-9, Cxcl-1, Cxcl-10 and Ccl20 (5) using qPCR (Fig.”
• Four faces of cellular senescence (2011, unknown): “(f) Senescent cells with persistent DDR signaling secrete growth factors, proteases, cytokines, and other factors that have potent autocrine and paracrine activities (Acosta et al., 2008; Coppé et al., 2008, 2010; Kuilman et al., 2008).”
• Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2015, methodology): “Cells induced to senesce by ionizing radiation (IR) (10 Gy), a common senescence inducer (Coppé et al., 2008; Rodier et al., 2009), showed no change in SIRT3 mRNA or protein (Figure S1D), indicating that reduced SIRT3 expression does not comprise the senescence response.”
• The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “SASP from senescent fibroblasts can strongly induce epithelium cells to proliferate, transform, and metastasize (Krtolica et al., 2001; Coppé et al., 2008).”
• Aging, Cellular Senescence, and Cancer (2012, background): “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).”