Cell Death & Differentiation (2018) 25:1005–1006 https://doi.org/10.1038/s41418-018-0102-y EDITORIAL Oncogene-induced senescence and tumour control in complex biological systems 1,2,3 4,5,6 Lorenzo Galluzzi Ilio Vitale Received: 6 March 2018 / Accepted: 9 March 2018 / Published online: 17 April 2018 © ADMC Associazione Differenziamento e Morte Cellulare 2018 Mammalian cells experiencing potentially oncogenic con- autophagy, an evolutionarily old mechanism of adaptation ditions can undergo regulated cell death (RCD)  as well that is particularly important for the metabolic reprogram- as an irreversible proliferative arrest known as cellular ming and survival of senescent cells , in a model of G12V senescence . Senescent cells are unable to proliferate HRAS -driven OIS. In the experimental setting G12V owing to the permanent upregulation of cell cycle inhibitors employed by Sulli and colleagues , however, HRAS , and are preferential targets for elimination by the overexpression results in approximately 60% of cells immune system . Thus, the net effect of senescence at the staining positively for senescence-associated β galactosi- cell-intrinsic level is robust oncosuppression. However, dase (as they report in Extended Data Fig. 9), implying that senescent cells also release multiple cytokines that may approximately 40% cells retained proliferative potential. support the proliferation of non-senescent
Cell Death & Differentiation – Springer Journals
Published: Apr 17, 2018
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