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. 2018 Apr 18;46(11):5504–5524. doi: 10.1093/nar/gky263

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© The Author(s) 2018. 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 8. — Model for TNBL expression in CRC. Acrocentric chromosomes 13, 14, 15 and 21 contain tandem arrays of NBL2 MSR, repressed by DNA methylation and histone deacetylation in normal colon epithelia. Upon NBL2 DNA hypomethylation TNBL lncRNA is expressed at moderate levels. Subsequent increase of histone acetylation results in high TNBL expression. TNBL location is nuclear where it mostly forms aggregates in the perinucleolar region close to NBL2 loci. These aggregates interact with SNB creating cancer-specific perinucleolar structures. Outside of the perinucleolar aggregates, TNBL is widely dispersed in the nucleus. Whether TNBL selective binding to NPM1, SAM68 and CELF1 proteins, which are involved in genome organization, splicing regulation and mRNA stability respectively, could impair their functionalities and potentially impact nuclear architecture and cell behavior is at the moment unknown.