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