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• W2034519672 abstract "NUT midline carcinoma (NMC) belongs to a class of highly lethal and poorly differentiated epithelial cancers arising mainly in human midline organs. NMC is caused by the chromosome translocation-mediated fusion of the <i>NUT</i> (nuclear protein in testis) gene on chromosome 15 to a few other genes, most frequently the <i>BRD4</i> gene on chromosome 19. The mechanism by which the <i>BRD4-NUT</i> fusion product blocks NMC cellular differentiation and contributes to oncogenesis remains elusive. In this study, we show that BRD4-NUT and BRD4 colocalize in discrete nuclear foci that are hyperacetylated but transcriptionally inactive. BRD4-NUT recruits histone acetyltransferases to induce histone hyperacetylation in these chromatin foci, which provide docking sites for accumulation of additional BRD4 and associated P-TEFB (positive transcription elongation factor b) complexes in the transcriptionally inactive BRD4-NUT foci. These molecular events lead to repression of a BRD4·P-TEFB downstream target gene c-<i>fos</i>, a component of activator protein 1 (AP-1), that directly regulates epithelial differentiation. Knockdown of <i>BRD4-NUT</i> in NMC cells disperses the transcriptionally inactive chromatin foci and releases the transcriptional activators to stimulate c-<i>fos</i> expression, leading to restoration of cellular differentiation. Our study provides a novel mechanism by which the <i>BRD4-NUT</i> oncogene perturbs BRD4 functions to block cellular differentiation and to contribute to the oncogenic progression in the highly aggressive NMC." @default.
• W2034519672 created "2016-06-24" @default.
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• W2034519672 date "2011-08-01" @default.
• W2034519672 modified "2023-10-09" @default.
• W2034519672 title "Perturbation of BRD4 Protein Function by BRD4-NUT Protein Abrogates Cellular Differentiation in NUT Midline Carcinoma" @default.
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• W2034519672 doi "https://doi.org/10.1074/jbc.m111.246975" @default.
• W2034519672 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3149357" @default.
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