Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 21, Issue 10, Pages 1256-1261Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612821666141211153853
Keywords
Twist; BRD4; epithelial-mesenchymal transition; basal-like breast cancer
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Funding
- NIH [CA125454]
- Mary Kay Ash Foundation
- Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health [P20 GM103527-06]
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As an important basic helix-loop-helix (bHLH) transcription factor, Twist associates with several physiological processes such as mesodermal development, and pathological processes such as Saethre-Chotzen syndrome. During cancer progression, Twist induces epithelial-mesenchymal transition (EMT), potentiating cancer cell invasion and metastasis. Although many studies have revealed its multiple biological roles, it remained unclear how Twist transcriptionally acti vates targeted genes. Recently we discovered tip60-mediated Twist di-acetylation in the histone H4-mimic'' GK-X-GK motif. The di-acetylated Twist recruits BRD4 and related transcriptional components to super-enhancer of its targeted genes during progression of basal-like breast cancer (BLBC). Here, we review this new advance of regulation and functional mechanism of Twist.
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