The essence of senescence

Abstract

Almost half a century after the first reports describing the limited replicative potential of primary cells in culture, there is now overwhelming evidence for the existence of "cellular senescence" in vivo. It is being recognized as a critical feature of mammalian cells to suppress tumorigenesis, acting alongside cell death programs. Here, we review the various features of cellular senescence and discuss their contribution to tumor suppression. Additionally, we highlight the power and limitations of the biomarkers currently used to identify senescent cells in vitro and in vivo.

Figure 1.

The essence of senescence: biomarkers in vivo. Several markers of cellular senescence have been identified in early neoplastic lesions in both mice and humans. Representative examples are shown in the various columns, with the type of genetic lesions or other types of stress (stress categories, color-coded) that instigate senescence at the very top and very bottom, and from thereon inward: the tissue types, specific stress signals, biomarkers, and symbols legends, respectively. For instance, in BRAF mutant nevi, the stress category is oncogene activation (blue), the tissue type is nevus, the specific stress signal is BRAF, and the biomarkers reported are cell cycle arrest, increase in SA-β-GAL activity, and tumor suppressor activation. (CTX) Cyclophosphamide; (βCAT) β-catenin; (GL) gland; (N.D.) not determined.