Journal
CANCER CELL
Volume 26, Issue 4, Pages 534-548Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2014.09.002
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Funding
- National Health Research Institutes [NHRI-EX103-10331BI]
- Ministry of Science and Technology [102-2321-B-010-006, 103-2321-B-010-019, 101-2314-B-010-021-MY3]
- Taipei Veterans General Hospital [V103-E8-002]
- Veterans General Hospitals-University System of Taiwan Joint Research Program [VGHUST103-G-7-5-1]
- Ministry of Education
- Ministry of Health and Welfare, Center of Excellence for Cancer Research [MOHW103-TD-B-111-02]
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Snail is primarily known as a transcriptional repressor that induces epithelial-mesenchymal transition by suppressing adherent proteins. Emerging evidence suggests that Snail can act as an activator; however, the mechanism and biological significance are unclear. Here, we found that CREB-binding protein (CBP) is the critical factor in Snail-mediated target gene transactivation. CBP interacts with Snail and acetylates Snail at lysine 146 and lysine 187, which prevents the repressor complex formation. We further identified several Snail-activated targets, including TNF-alpha, which is also the upstream signal for Snail acetylation, and CCL2 and CCL5, which promote the recruitment of tumor-associated macrophages. Here, we present our results on the mechanism by which Snail induces target gene transactivation to remodel the tumor microenvironment.
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