Abstract

Abstract The ageing process is a highly complex eventual outcome of development. Cancer is a disease of multicellular organisms that results primarily due to uncontrolled cell proliferation. Although cancer is a pathological phenomenon, ageing by itself is a natural process. However, ageing can promote certain age‐related pathologies including cancer. Both cancer and the ageing process have deleterious effects on the well‐being of an organism. At the cellular level, a complex phenotype known as cellular senescence regulates both cancer and the ageing process. A cell undergoes senescence due to telomere shortening or exposure to various stress factors. Senescent cells are morphologically and functionally distinct from proliferating and apoptotic cells. These cells do not divide but are metabolically active. In the context of a tissue or an organ, senescent cells exert both cell autonomous and nonautonomous effects, which regulate cancer and the ageing process. Key Concepts: Ageing is the key risk factor for cancer and it promotes cancer. All normal cells undergo cellular senescence, a permanent growth‐arrested phase. Cellular senescence results due to intrinsic factors such as telomere shortening or extrinsic factors such as stress. Induction of senescence by intrinsic or extrinsic factors is mediated by p53/p21 and p16INK4A/pRB tumour suppressor pathways. Tumour suppressor pathways not only regulate cancer but also regulate organismic ageing. Cellular senescence contributes to ageing and cancer via its cell autonomous and nonautonomous effects. Cellular senescence can suppress or promote cancer via cell autonomous and nonautonomous mechanisms. Model systems can be used to study the mechanism of ageing and cancer.

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