德国研究人员周一表示，发现了一种参与细胞分裂的基因，该基因与神经母细胞瘤(neuroblastoma)有关，此结果为研制相关治疗药物提供了新方法。
神经母细胞瘤是一种可致命的小儿恶性肿瘤。
研究人员在《癌细胞》期刊上撰文指出，AURKA基因产生的蛋白质为另一种名为MYCN的基因提供养料。而MYCN基因对神经母细胞瘤生长起关键作用。
德国乌兹堡大学的Martin Eilers是本次研究的带头人，他在接受电话采访时表示，“目前还没有制药公司有能力针对MYCN基因进行研发，我们的发现为开发新药攻克神经母细胞瘤提供了希望。”
在患癌症而死的儿童中，神经母细胞瘤患者占了15%。这种癌症的存活率只有40%，尽管神经母细胞瘤患者只占所有小儿癌症患者的7%。
Eilers及其研究团队对患儿体内与MYCN有关的200种基因进行了筛查，结果发现AURKA基因产生的蛋白对癌细胞生长起了重要作用。（生物谷Bioon.com）
生物谷推荐原始出处：
Cancer Cell, Volume 15, Issue 1, 67-78, 6 January 2009 doi:10.1016/j.ccr.2008.12.005
Stabilization of N-Myc Is a Critical Function of Aurora A in Human Neuroblastoma
Tobias Otto1,Sebastian Horn1,Markus Brockmann1,Ursula Eilers1,Lars Schüttrumpf1,Nikita Popov1,Anna Marie Kenney2,Johannes H. Schulte3,Roderick Beijersbergen4,Holger Christiansen5,Bernd Berwanger5,6andMartin Eilers1,6,7,,
1 Institute of Molecular Biology and Tumor Research, Emil-Mannkopf-Strae 2, 35037 Marburg, Germany
2 Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
3 Department of Pediatric Hematology, Oncology and Endocrinology, University Hospital of Essen, 45122 Essen, Germany
4 Netherlands Cancer Center, Plesmanlaan 121, Amsterdam CX 1066, The Netherlands
5 Children's Hospital, Medical Center, Philipps-Universit?t Marburg, Baldingerstrae, 35043 Marburg, Germany
6 These authors contributed equally to this work
7 Present address: Department of Physiological Chemistry, Biocenter, Universit?t Würzburg, Am Hubland, 97074 Würzburg, Germany
In human neuroblastoma, amplification of the MYCN gene predicts poor prognosis and resistance to therapy. In a shRNA screen of genes that are highly expressed in MYCN-amplified tumors, we have identified AURKA as a gene that is required for the growth of MYCN-amplified neuroblastoma cells but largely dispensable for cells lacking amplified MYCN. Aurora A has a critical function in regulating turnover of the N-Myc protein. Degradation of N-Myc requires sequential phosphorylation by cyclin B/Cdk1 and Gsk3. N-Myc is therefore degraded during mitosis in response to low levels of PI3-kinase activity. Aurora A interacts with both N-Myc and the SCFFbxw7 ubiquitin ligase that ubiquitinates N-Myc and counteracts degradation of N-Myc, thereby uncoupling N-Myc stability from growth factor-dependent signals.
