Abstract
Cellular senescence is a state of irreversible cell proliferation arrest provoked by a persistent DNA damage induced by a variety of potentially oncogenic signals, and it was initially identified as a tumour-suppression mechanism. Recent studies, however, revealed that senescent cells have the potential to secrete numerous inflammatory cytokines, chemokines, growth factors, and matrix-remodeling factors, because unlike apoptotic cells, senescent cells are viable for a long period of time. This newly identified phenotype of cellular senescence, called senescence-associated secretory phenotype (SASP or senescence-associated secretome), could potentially provide beneficial effects, such as reinforcement of cellular senescence and tissue repair, but sometimes could induce deleterious side effects, such as chronic inflammation and cancer progression, depending on the biological context. Since obesity is associated with chronic inflammation and cancer, we thought that the senescence-associated secretome could be closely involved in the inflammation and tumourigenesis accompanying obesity. In this review, I first discuss the role and the mechanism of cellular senescence, and then introduce the role of senescence-associated secretome in vivo including our recent findings on the mechanism of obesity-associated liver cancer, promoted by the senescence-associated secretome in hepatic stellate cells, which could form a cancer-promoting microenvironment.
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Ohtani, N. (2016). Cellular Senescence as a Novel Mechanism of Chronic Inflammation and Cancer Progression. In: Miyasaka, M., Takatsu, K. (eds) Chronic Inflammation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56068-5_15
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