Yamauchi Shota, Takahashi Akiko
Division of Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550, Japan.
Cancer Cell Communication Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550, Japan.
J Biochem. 2025 Mar 4;177(3):163-169. doi: 10.1093/jb/mvae079.
Cellular senescence is an irreversible cell cycle arrest induced by stresses such as telomere shortening and oncogene activation. It acts as a tumor suppressor mechanism that prevents the proliferation of potentially tumorigenic cells. Paradoxically, senescent stromal cells that arise in the tumor microenvironment have been shown to promote tumor progression. In addition, senescent cells that accumulate in vivo over time are thought to contribute to aging and age-related diseases. These deleterious effects of senescent cells involve the secretion of bioactive molecules such as inflammatory cytokines and chemokines, a phenomenon known as the senescence-associated secretory phenotype. While the role of cellular senescence in vivo is becoming increasingly clear, the intracellular signaling pathways that induce the expression of senescent phenotypes are not fully understood. In this review, we outline senescence-associated signaling pathways and their relevance to cancer and aging.
细胞衰老指的是由端粒缩短和癌基因激活等应激诱导的不可逆细胞周期停滞。它作为一种肿瘤抑制机制，可阻止潜在致瘤细胞的增殖。矛盾的是，肿瘤微环境中出现的衰老基质细胞已被证明会促进肿瘤进展。此外，随着时间推移在体内积累的衰老细胞被认为与衰老及衰老相关疾病有关。衰老细胞的这些有害作用涉及炎性细胞因子和趋化因子等生物活性分子的分泌，这一现象被称为衰老相关分泌表型。虽然细胞衰老在体内的作用日益清晰，但诱导衰老表型表达的细胞内信号通路尚未完全明确。在本综述中，我们概述了衰老相关信号通路及其与癌症和衰老的相关性。
