衰老和癌症。

Cancer Translational Medicine Pub Date : 2018-05-01 Epub Date: 2018-06-29 DOI:10.4103/ctm.ctm_22_18
Sulin Zeng, Wen H Shen, Li Liu
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引用次数: 58

摘要

衰老是一把双刃剑,可以在相反的方向发挥作用。这是细胞避免恶性转化的一种潜在机制。然而,衰老也可以通过衰老相关分泌表型(SASP)改变细胞微环境,从而促进癌症的发展。至少有三种类型的细胞应激,如癌基因的激活、肿瘤抑制基因的缺失和化疗/放疗可诱导细胞衰老。癌基因诱导的衰老可能与复制性衰老交织在一起。早期的衰老可以保护细胞免于转化,而延长的衰老往往促进癌症的发展。本文将重点介绍衰老的特征,讨论衰老在癌症发展过程中的调控作用,并强调衰老的复杂性给癌症治疗带来了挑战。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Senescence and Cancer.

Senescence is a double-edged sword that can function in opposite directions. It is a potential mechanism for a cell to avoid malignant transformation. However, senescence can also promote cancer development by altering the cellular microenvironment through a senescence-associated secretory phenotype (SASP). At least, three types of cellular stress such as activation of oncogenes, loss of tumor suppressor genes, and chemo/radiotherapy can induce cell senescence. Oncogene-induced senescence can be intertwiningly associated with the replicative senescence. Early-stage senescence may protect cell from transformation, while prolonged senescence often promotes cancer development. This review will focus on the characteristics of senescence, discuss the regulation of senescence during cancer development, and highlight the complexity of senescence that makes cancer treatment challenging.

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