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Aurora kinases A and B are up-regulated by Myc and are essential for maintenance of the malignant state
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
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2010 (engelsk)Inngår i: Blood, ISSN 0006-4971, E-ISSN 1528-0020, Vol. 116, nr 9, s. 1498-1505Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Myc oncoproteins promote continuous cell growth, in part by controlling the transcription of key cell cycle regulators. Here, we report that c-Myc regulates the expression of Aurora A and B kinases (Aurka and Aurkb), and that Aurka and Aurkb transcripts and protein levels are highly elevated in Myc-driven B-cell lymphomas in both mice and humans. The induction of Aurka by Myc is transcriptional and is directly mediated via E-boxes, whereas Aurkb is regulated indirectly. Blocking Aurka/b kinase activity with a selective Aurora kinase inhibitor triggers transient mitotic arrest, polyploidization, and apoptosis of Myc-induced lymphomas. These phenotypes are selectively bypassed by a kinase inhibitor-resistant-Aurkb mutant, demonstrating that Aurkb is the primary therapeutic target in the context of Myc. Importantly, apoptosis provoked by Aurk inhibition was p53 independent, suggesting that Aurka/Aurkb inhibitors will show efficacy in treating primary or relapsed malignancies having Myc involvement and/or loss of p53 function. (Blood. 2010;116(9):1498-1505)

sted, utgiver, år, opplag, sider
2010. Vol. 116, nr 9, s. 1498-1505
Emneord [en]
c-myc, transcriptional control, dna-replication, growth arrest, target genes, in-vivo, apoptosis, suppression, progression, inhibitor
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-43181DOI: 10.1182/blood-2009-11-251074ISI: 000281572700017OAI: oai:DiVA.org:umu-43181DiVA, id: diva2:412352
Tilgjengelig fra: 2011-04-22 Laget: 2011-04-22 Sist oppdatert: 2018-06-08bibliografisk kontrollert

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