Stress-induced Cellular Senescence Contributes to Chronic Inflammation and Cancer Progression
Stress-induced Cellular Senescence Contributes to Chronic Inflammation and Cancer Progression
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DOI：
10.3191/thermalmed.35.41
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发表时间：
2019-12
期刊：
影响因子：
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通讯作者：
Shinko Kobashigawa;Yoshihiko M. Sakaguchi;S. Masunaga;Eiichiro Mori
中科院分区：
文献类型：
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作者：
Shinko Kobashigawa;Yoshihiko M. Sakaguchi;S. Masunaga;Eiichiro Mori
细胞衰老长期以来被认为是一种肿瘤抑制因子或肿瘤抑制机制，并被描述为一种不可逆的细胞周期停滞现象。然而，细胞衰老现在被认为具有肿瘤抑制以外的生理功能;已经发现它参与胚胎发生、组织/器官老化和伤口愈合。令人惊讶的是，细胞衰老也被证明在某些情况下具有肿瘤进展作用。衰老细胞表现出称为衰老相关分泌表型（SASP）的分泌表型，其分泌多种SASP因子，包括炎性细胞因子、趋化因子和生长因子，以及促进邻近组织微环境改变的基质重塑因子。已知这种SASP因子驱动细胞衰老的多效性特征的机制。在这篇综述中，我们在分子和细胞水平上研究了当前对细胞衰老的认识，重点是慢性炎症和肿瘤进展。
Cellular senescence has long been considered to act as a tumor suppressor or tumor suppression mechanism and described as a phenomenon of irreversible cell cycle arrest. Cellular senescence, however, is now considered to have physiological functions other than tumor suppression; it has been found to be involved in embryogenesis, tissue/organ aging, and wound healing. Surprisingly, cellular senescence is also demonstrated to have a tumor progressive role in certain situations. Senescent cells exhibit secretory phenotypes called senescence-associated secretory phenotype (SASP), which secrete a variety of SASP factors including inflammatory cytokines, chemokines, and growth factors, as well as matrix remodeling factors that promote the alteration of neighboring tissue microenvironments. Such SASP factors have been known to drive the mechanisms underlying the pleiotropic features of cellular senescence. In this review, we examine current knowledge of cellular senescence at molecular and cellular levels, with a focus on chronic inflammation and tumor progression.