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Impact of senescence‐associated secretory phenotype and its potential as a therapeutic target for senescence‐associated diseases
Author(s) -
Watanabe Sugiko,
Kawamoto Shimpei,
Ohtani Naoko,
Hara Eiji
Publication year - 2017
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13184
Subject(s) - senescence , biology , carcinogenesis , phenotype , microbiology and biotechnology , secretion , context (archaeology) , chemokine , cell cycle checkpoint , proinflammatory cytokine , cell cycle , immunology , cell , cancer research , inflammation , cancer , genetics , endocrinology , gene , paleontology
“Cellular senescence” is a state in which cells undergo irreversible cell cycle arrest in response to a variety of cellular stresses. Once cells senesce, they are strongly resistant to any mitogens, including oncogenic stimuli. Therefore, cellular senescence has been assumed to be a potent anticancer mechanism. Although irreversible cell‐cycle arrest is traditionally considered the major characteristic of senescent cells, recent studies have revealed some additional functions. Most noteworthy is the increased secretion of various secretory proteins, such as inflammatory cytokines, chemokines, growth factors, and MMP s, into the surrounding extracellular fluid. These newly recognized senescent phenotypes, termed senescence‐associated secretory phenotypes ( SASP s), reportedly contribute to tumor suppression, wound healing, embryonic development, and even tumorigenesis promotion. Thus, SASP s appear to be beneficial or deleterious, depending on the biological context. As senescent cells are known to accumulate during the aging process in vivo , it is quite possible that their accumulation in aged tissues promotes age‐associated functional decline and various diseases, including cancers, at least to some extent. Here, we focus on and discuss the functional and regulatory network of SASP s toward opening up new possibilities for controlling aging and aging‐associated diseases.

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