Abstract
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.
Original language | English |
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Pages (from-to) | 1256-1261 |
Number of pages | 6 |
Journal | Current Pharmaceutical Design |
Volume | 21 |
Issue number | 10 |
DOIs | |
State | Published - Jan 1 2015 |
Bibliographical note
Publisher Copyright:© 2015 Bentham Science Publishers.
Funding
Funders | Funder number |
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National Institute of General Medical Sciences | |
National Institutes of Health (NIH) | P20 GM103527-06, CA125454 |
National Institute of General Medical Sciences | P20GM103527 |
Keywords
- BRD4
- Basal-like breast cancer
- Epithelial-mesenchymal transition
- Twist
ASJC Scopus subject areas
- Pharmacology
- Drug Discovery