晨间信号Morning Signal
《科学》 2026年10月1日 · 中文解读

抑癌基因关闭信号梯度

A tumor suppressor shuts down a signal gradient · D. Engelman and C. Blanpain
约 9 分钟Perspectives在小程序里点播,20 到 60 分钟做好
这篇讲什么
Gan等人在《科学》杂志报告,p53缺失导致小鼠表皮突变克隆内形成Wnt活性梯度,中心最高、向边缘递减,从而驱动克隆扩增。p53通过激活Sfrp1、Lrp1和Usp22三个Wnt抑制因子来阻止这一梯度的建立。该发现表明,控制信号梯度而非信号绝对量,可能是癌症相关突变实现组织长期定植的机制。
原文开头
p53 shuts down the spatial signaling of a morphogen and prevents clonal cell expansion Dan Engelman1 and Cédric Blanpain1,2 The most frequently mutated tumor suppressor gene in human cancers is TP53 (1). Loss-of-function mutations lead to expansion of a mutated cell and its progeny in epithelial tissues, including sun-exposed regions of the skin, which can progress to invasive cancers. Upon stress, such as DNA damage, p53 becomes phosphorylated or acetylated, modifications that promote its stabilization and the activation of genes that cause cell cycle arrest, cellular senescence, or cell death (1). One might expect that clonal expansion triggered by the loss of p53 results from dysregulation of these canonical functions. On page 78 of this issue, Gan et al. …
摘自《科学》(Science)2026年10月1日,D. Engelman and C. Blanpain。仅引用开头一小段供了解文章,版权归原刊所有,全文请阅读原刊。
晨间信号小程序码
微信扫码,在小程序里听完整版
不用登录先听一篇 · 或在微信搜索小程序 晨间信号
同期其他文章