Normal primary cells proliferate in culture for a limited number of population doublings prior to undergoing terminal growth arrest and acquiring a senescent phenotype. This finite life span correlates with the age of the organism and with the life expectancy of the species from which the cells were obtained. The older the age or the shorter the life span, the less the ability of the cells to undergo population doubling.
Senescent cells are characterized by an irreversible G1 growth arrest involving the repression of genes that drive cell cycle progression and the upregulation of cell cycle inhibitors like p16INK4a, p53, and its transcriptional target, p21CIP1. They are resistant to mitogen induced proliferation, and assume a characteristic enlarged, flattened morphology. Research into the pathways that positively regulate senescence and ways cells bypass senescence is therefore critical in understanding carcinogenesis. Normal cells have several mechanisms in place to protect against uncontrolled proliferation and tumorigenesis.
Senescent cells show common biochemical markers such as expression of an acidic senescence-associated β-galactosidase (SA-β-gal) activity. While senescence has been characterized primarily in cultured cells, there is also evidence that it occurs in vivo. Cells expressing markers of senescence such as SA-β-gal have been identified in normal tissues.
UniProt ID:
P16278
Regulatory Status:
RUO - Research Use Only
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