Myc proteins as therapeutic targets

被引：162

作者：

Gustafson, W. C. ^{[1
,2
]}

Weiss, W. A. ^{[1
,3
,4
]}

机构：

[1] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94158 USA

[2] Univ Calif San Francisco, Div Pediat Hematol Oncol, San Francisco, CA 94143 USA

[3] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA

[4] Univ Calif San Francisco, Dept Neurosurg, San Francisco, CA 94143 USA

来源：

ONCOGENE | 2010年 / 29卷 / 09期

关键词：

myc; mycn; neuroblastoma; N-myc; mTor; PI3K; ANAPLASTIC LYMPHOMA KINASE; INITIAL TESTING STAGE-1; ARF TUMOR-SUPPRESSOR; C-MYC; N-MYC; GENE-EXPRESSION; DNA-BINDING; CELL-LINES; TRANSCRIPTIONAL CONTROL; MALIGNANT PROGRESSION;

D O I：

10.1038/onc.2009.512

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Myc proteins (c-myc, Mycn and Mycl) target proliferative and apoptotic pathways vital for progression in cancer. Amplification of the MYCN gene has emerged as one of the clearest indicators of aggressive and chemotherapy-refractory disease in children with neuroblastoma, the most common extracranial solid tumor of childhood. Phosphorylation and ubiquitin-mediated modulation of Myc protein influence stability and represent potential targets for therapeutic intervention. Phosphorylation of Myc proteins is controlled in-part by the receptor tyrosine kinase/phosphatidylinositol 3-kinase/Akt/mTOR signaling, with additional contributions from Aurora A kinase. Myc proteins regulate apoptosis in part through interactions with the p53/Mdm2/Arf signaling pathway. Mutation in p53 is commonly observed in patients with relapsed neuroblastoma, contributing to both biology and therapeutic resistance. This review examines Myc function and regulation in neuroblastoma, and discusses emerging therapies that target Mycn. Oncogene (2010) 29, 1249-1259; doi:10.1038/onc.2009.512; published online 25 January 2010

引用

页码：1249 / 1259

页数：11

共 202 条

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