The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Disrupting the Interaction of BRD4 with Diacetylated Twist Suppresses Tumorigenesis in Basal-like Breast Cancer
Open accessAbstract
Summary Twist is a key transcription activator of epithelial-mesenchymal transition (EMT). It remains unclear how Twist induces gene expression. Here we reported a mechanism by which Twist recruits BRD4 to direct WNT5A expression in basal-like breast cancer (BLBC). Twist contains a “histone H4 mimic” GK-X-GK motif that is di-acetylated by Tip60. The di-acetylated Twist binds the second bromodomain of BRD4, whose first bromodomain interacts with acetylated H4, thereby constructs an activated Twist/BRD4/P-TEFb/RNA-PolII complex at the WNT5A promoter and enhancer. Pharmacologic inhibition of the Twist-BRD4 association reduced WNT5A expression and suppressed invasion, cancer stem cell (CSC)-like properties, and tumorigenicity of BLBC cells. Our study indicates that the interaction with BRD4 is critical for the oncogenic function of Twist in BLBC.
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Cited by
Functions and mechanisms of non-histone protein acetylation
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BET Proteins as Targets for Anticancer Treatment
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Metadata
- Authors
- Shi, J., Wang, Y., Zeng, L., Wu, Y., Deng, J., Zhang, Q., Lin, Y., Li, J., Kang, T., Tao, M., Rusinova, E., Zhang, G., Wang, C., Zhu, H., Yao, J., Zeng, Y.-X., Evers, B. M., Zhou, M.-M., & Zhou, B. P.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2014-02
- Volume
- 25
- Issue
- 2
- Pages
- 210-225
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W1966227037
- Cited by
- 477
- References
- 30
- FWCI
- 16.67
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Shi, J., Wang, Y., Zeng, L., Wu, Y., Deng, J., Zhang, Q., Lin, Y., Li, J., Kang, T., Tao, M., Rusinova, E., Zhang, G., Wang, C., Zhu, H., Yao, J., Zeng, Y.-X., Evers, B. M., Zhou, M.-M., & Zhou, B. P. (2014). Disrupting the Interaction of BRD4 with Diacetylated Twist Suppresses Tumorigenesis in Basal-like Breast Cancer. Cancer Cell. https://doi.org/10.1016/j.ccr.2014.01.028
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