期刊
CELL REPORTS
卷 5, 期 6, 页码 1679-1689出版社
CELL PRESS
DOI: 10.1016/j.celrep.2013.11.034
关键词
-
类别
资金
- Howard Hughes Medical Institute
- NIH [CA129933]
- Susan G. Komen for the Cure
- NCI-MGH Federal Share Program
- Ellison Medical Foundation [AG-NS-0560-09, CA059267, R01GM097360]
- Jane Coffin Childs Memorial Fund for Medical Research
Epithelial-mesenchymal transition (EMT) is thought to contribute to cancer metastasis, but its underlying mechanisms are not well understood. To define early steps in this cellular transformation, we analyzed human mammary epithelial cells with tightly regulated expression of Snail-1, a master regulator of EMT. After Snail-1 induction, epithelial markers were repressed within 6 hr, and mesenchymal genes were induced at 24 hr. Snail-1 binding to its target promoters was transient (6-48 hr) despite continued protein expression, and it was followed by both transient and long-lasting chromatin changes. Pharmacological inhibition of selected histone acetylation and demethylation pathways suppressed the induction as well as the maintenance of Snail-1-mediated EMT. Thus, EMT involves an epigenetic switch that may be prevented or reversed with the use of small-molecule inhibitors of chromatin modifiers.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据