[衰老与癌症]。
[Senescence and Cancer].
发表日期：2024 Aug
作者：
Tomonori Matsumoto, Eiji Hara
来源：
Cell Death & Disease
摘要：
经历重大压力（例如不可修复的基因组损伤）的细胞会进入一种称为细胞衰老的状态，其中细胞周期被不可逆转地停滞。最初，细胞衰老被认为是通过阻止可能导致癌症发展的异常细胞的生长来抑制癌变的关键机制。然而，显而易见的是，化疗等治疗诱导的衰老可以通过表现出对细胞死亡的抵抗力并允许癌细胞存活来促进癌症的耐药性。此外，衰老细胞表现出一种称为衰老相关分泌表型（SASP）的特性，它们释放多种炎症分子和生长因子。通过这些影响肿瘤微环境的SASP因子，衰老细胞可以深入参与多种癌症病理过程，例如癌变和耐药性的获得。本文概述了细胞衰老与癌症发生和进展之间多方面且复杂的相互作用。
Cells experiencing significant stress such as irreparable genomic damage enter a state called cellular senescence, where their cell cycle is irreversibly arrested. Originally, cellular senescence was thought to serve as a crucial mechanism for suppressing carcinogenesis by stopping the growth of abnormal cells that could potentially lead to cancer development. However, it has become evident that senescence induced by treatments such as chemotherapy can contribute to drug resistance in cancer by exhibiting resistance to cell death and allowing cancer cells to survive. Furthermore, senescent cells exhibit a property known as the senescence-associated secretory phenotype(SASP), where they release a variety of inflammatory molecules and growth factors. Through these SASP factors influencing the tumor microenvironment, senescent cells can be deeply involved in various cancer pathologies such as carcinogenesis and the acquisition of drug resistance. This article provides an overview of the multifaceted and complex interplay between cellular senescence and the initiation and progression of cancer.