德國(guó)研究人員周一表示,，發(fā)現(xiàn)了一種參與細(xì)胞分裂的基因,，該基因與神經(jīng)母細(xì)胞瘤(neuroblastoma)有關(guān),，此結(jié)果為研制相關(guān)治療藥物提供了新方法。
神經(jīng)母細(xì)胞瘤是一種可致命的小兒惡性腫瘤,。
研究人員在《癌細(xì)胞》期刊上撰文指出,，AURKA基因產(chǎn)生的蛋白質(zhì)為另一種名為MYCN的基因提供養(yǎng)料。而MYCN基因?qū)ι窠?jīng)母細(xì)胞瘤生長(zhǎng)起關(guān)鍵作用,。
德國(guó)烏茲堡大學(xué)的Martin Eilers是本次研究的帶頭人,，他在接受電話(huà)采訪時(shí)表示，“目前還沒(méi)有制藥公司有能力針對(duì)MYCN基因進(jìn)行研發(fā),，我們的發(fā)現(xiàn)為開(kāi)發(fā)新藥攻克神經(jīng)母細(xì)胞瘤提供了希望,。”
在患癌癥而死的兒童中，神經(jīng)母細(xì)胞瘤患者占了15%,。這種癌癥的存活率只有40%,，盡管神經(jīng)母細(xì)胞瘤患者只占所有小兒癌癥患者的7%。
Eilers及其研究團(tuán)隊(duì)對(duì)患兒體內(nèi)與MYCN有關(guān)的200種基因進(jìn)行了篩查,，結(jié)果發(fā)現(xiàn)AURKA基因產(chǎn)生的蛋白對(duì)癌細(xì)胞生長(zhǎng)起了重要作用,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
