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. 2020 Nov 16;48(21):12135–12150. doi: 10.1093/nar/gkaa1051

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© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 7. — Silencing EP300 abolishes H3K27 acetylation at the NTS locus and inhibits NTS expression. (A) ChIP assay of the H3K27Ac status in the NTS promoter and its enhancer region after siRNA EP300 transfection in UM cells. (B) qRT-PCR showed that NTS was silenced after silencing EP300 in UM cells. *P< 0.05, **P< 0.01. (C) Western blot was performed to detect NTS protein expression after silencing EP300 in UM cells. (D) Schematic diagram of the research model. CTCF interacts with distal enhancers to form chromosomal loops and recruits the histone acetyltransferase EP300 to activate the oncogene NTS and contributes to tumor progression. The targeted correction of abnormal NTS-LRRIQ1 chromosomal interactions significantly inhibited tumorigenesis by deleting oncogenic enhancers or inactivating histone acetyltransferases.