MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.

Doose, Gero, Haake, Andrea, Bernhart, Stephan H., Lopez, Cristina, Duggimpudi, Sujitha, Wojciech, Franziska, Bergmann, Anke K., Borkhardt, Arndt, Burkhardt, Birgit, Claviez, Alexander, Dimitrova, Lora, Haas, Siegfried, Hoell, Jessica I., Hummel, Michael, Karsch, Dennis, Klapper, Wolfram, Kleo, Karsten, Kretzmer, Helene, Kreuz, Markus, Kueppers, Ralf, Lawerenz, Chris, Lenze, Dido, Loeffler, Markus, Mantovani-Loeffler, Luisa, Moeller, Peter, Ott, German, Richter, Julia, Rohde, Marius, Rosenstiel, Philip, Rosenwald, Andreas, Schilhabel, Markus, Schneider, Markus, Scholz, Ingrid, Stilgenbauer, Stephan, Stunnenberg, Hendrik G., Szczepanowski, Monika, Truemper, Lorenz, Weniger, Marc A., Hoffmann, Steve, Siebert, Reiner, Iaccarino, Ingram and Consortium, Icgc Mmml- Seq (2015) MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells. PNAS Proceedings of the National Academy of Sciences of the United States of America, 112 (38). E5261-E5270. DOI 10.1073/pnas.1505753112.

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Supplementary data:


Despite the established role of the transcription factor MYC in cancer, little is known about the impact of a new class of transcriptional regulators, the long noncoding RNAs (lncRNAs), on MYC ability to influence the cellular transcriptome. Here, we have intersected RNA-sequencing data from two MYC-inducible cell lines and a cohort of 91 B-cell lymphomas with or without genetic variants resulting in MYC overexpression. We identified 13 lncRNAs differentially expressed in IG-MYC-positive Burkitt lymphoma and regulated in the same direction by MYC in the model cell lines. Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Differential gene expression analysis after RNAi showed a significant enrichment of cell cycle genes among the genes down-regulated after MINCR knockdown. Interestingly, these genes are enriched in MYC binding sites in their promoters, suggesting that MINCR acts as a modulator of the MYC transcriptional program. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A and B and chromatin licensing and DNA replication factor 1 may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.

Document Type: Article
Additional Information: Times Cited: 4
Keywords: MYC, lncRNA, cell cycle, B-cell lymphoma
Research affiliation: Kiel University
Kiel University > Kiel Marine Science
OceanRep > The Future Ocean - Cluster of Excellence
Refereed: Yes
Open Access Journal?: No
DOI etc.: 10.1073/pnas.1505753112
ISSN: 0027-8424
Projects: Future Ocean
Date Deposited: 20 Oct 2016 10:54
Last Modified: 23 Sep 2019 20:18
URI: http://oceanrep.geomar.de/id/eprint/32455

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