Small molecule inhibitors of Aurora-A induce proteasomal degradation of N-Myc in childhood neuroblastoma
Amplification of MYCN is a driver mutation in a subset of human neuroendocrine tumors, including neuroblastoma. No small molecules that target N-Myc, the protein encoded by MYCN, are clinically available. N-Myc forms a complex with the Aurora-A kinase, which protects N-Myc from proteasomal degradati...
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| Hauptverfasser: | , , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
June 20, 2013
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| In: |
Cancer cell
Year: 2013, Jahrgang: 24, Heft: 1, Pages: 75-89 |
| ISSN: | 1878-3686 |
| DOI: | 10.1016/j.ccr.2013.05.005 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.ccr.2013.05.005 Verlag, lizenzpflichtig, Volltext: http://www.sciencedirect.com/science/article/pii/S1535610813002328 
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| Verfasserangaben: | Markus Brockmann, Evon Poon, Teeara Berry, Anne Carstensen, Hedwig E. Deubzer, Lukas Rycak, Yann Jamin, Khin Thway, Simon P. Robinson, Frederik Roels, Olaf Witt, Matthias Fischer, Louis Chesler, and Martin Eilers |
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| 520 | |a Amplification of MYCN is a driver mutation in a subset of human neuroendocrine tumors, including neuroblastoma. No small molecules that target N-Myc, the protein encoded by MYCN, are clinically available. N-Myc forms a complex with the Aurora-A kinase, which protects N-Myc from proteasomal degradation. Although stabilization of N-Myc does not require the catalytic activity of Aurora-A, we show here that two Aurora-A inhibitors, MLN8054 and MLN8237, disrupt the Aurora-A/N-Myc complex and promote degradation of N-Myc mediated by the Fbxw7 ubiquitin ligase. Disruption of the Aurora-A/N-Myc complex inhibits N-Myc-dependent transcription, correlating with tumor regression and prolonged survival in a mouse model of MYCN-driven neuroblastoma. We conclude that Aurora-A is an accessible target that makes destabilization of N-Myc a viable therapeutic strategy. | ||
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