The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma
Open accessAbstract
NUT midline carcinoma (NMC) is an aggressive type of squamous cell carcinoma that is defined by the presence of BRD-NUT fusion oncogenes, which encode chimeric proteins that block differentiation and maintain tumor growth. BRD-NUT oncoproteins contain two bromodomains whose binding to acetylated histones is required for the blockade of differentiation in NMC, but the mechanisms by which BRD-NUT act remain uncertain. Here, we provide evidence that MYC is a key downstream target of BRD4-NUT. Expression profiling of NMCs shows that the set of genes whose expression is maintained by BRD4-NUT is highly enriched for MYC upregulated genes, and MYC and BRD4-NUT protein expression is strongly correlated in primary NMCs. More directly, we find that BRD4-NUT associates with the MYC promoter and is required to maintain MYC expression in NMC cell lines. Moreover, both siRNA knockdown of MYC and a dominant-negative form of MYC, omomyc, induce differentiation of NMC cells. Conversely, differentiation of NMC cells induced by knockdown of BRD4-NUT is abrogated by enforced expression of MYC. Together, these findings suggest that MYC is a downstream target of BRD4-NUT that is required for maintenance of NMC cells in an undifferentiated, proliferative state. Our findings support a model in which dysregulation of MYC by BRD-NUT fusion proteins has a central role in the pathogenesis of NMC.
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Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Selective inhibition of BET bromodomains
Filippakopoulos, P., Qi, J., Picaud, S., Shen, Y., Smith, W. B., Fedorov, O., Morse, E. M., Keates, T., Hickman, T. T., Felletar, I., et al. (2010) · Nature · doi:10.1038/nature09504 · Cited by 4,262
Self-citationArnold, I., & Watt, F. M. (2001) · Current Biology · doi:10.1016/s0960-9822(01)00154-3 · Cited by 341
MYC in mammalian epidermis: how can an oncogene stimulate differentiation?
Watt, F. M., Frye, M., & Benitah, S. A. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2328 · Cited by 157
Cited by
Lysine Acetylation Goes Global: From Epigenetics to Metabolism and Therapeutics
Ali, I., Conrad, R. J., Verdin, E., & Ott, M. (2018) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00181 · Cited by 366
Marked for death: Targeting epigenetic changes in cancer
Pfister, S. X., & Ashworth, A. (2017) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2016.256 · Cited by 288
BET inhibitor OTX015 targets BRD2 and BRD4 and decreases c-MYC in acute leukemia cells
Coudé, M.-M., Braun, T., Berrou, J., Dupont, M., Bertrand, S., Masse, A., Raffoux, E., Itzykson, R., Delord, M., Riveiro, M. E., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.4131 · Cited by 274
Metadata
- Authors
- Grayson, A. R., Walsh, E. M., Cameron, M. J., Godec, J., Ashworth, T., Ambrose, J. M., Aserlind, A. B., Wang, H., Evan, G. I., Kluk, M. J., Bradner, J. E., Aster, J. C., & French, C. A.
- Venue
- Oncogene
- Published
- 2013-04-22
- Volume
- 33
- Issue
- 13
- Pages
- 1736-1742
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W1998469647
- Cited by
- 184
- References
- 4
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- green
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- The paper
- Grayson, A. R., Walsh, E. M., Cameron, M. J., Godec, J., Ashworth, T., Ambrose, J. M., Aserlind, A. B., Wang, H., Evan, G. I., Kluk, M. J., Bradner, J. E., Aster, J. C., & French, C. A. (2014). MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma. Oncogene. https://doi.org/10.1038/onc.2013.126
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