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本文引用的文献

1
A SUMOylation Motif in Aurora-A: Implications for Spindle Dynamics and Oncogenesis.SUMOylation 基序在 Aurora-A 中的作用：对纺锤体动力学和肿瘤发生的影响。
Front Oncol. 2011 Dec 14;1:50. doi: 10.3389/fonc.2011.00050. eCollection 2011.
2
Calmodulin activation of Aurora-A kinase (AURKA) is required during ciliary disassembly and in mitosis.钙调蛋白对极光激酶 A（AURKA）的激活作用在纤毛解体和有丝分裂过程中是必需的。
Mol Biol Cell. 2012 Jul;23(14):2658-70. doi: 10.1091/mbc.E11-12-1056. Epub 2012 May 23.
3
Pten regulates Aurora-A and cooperates with Fbxw7 in modulating radiation-induced tumor development.PTEN 调节 Aurora-A，并与 Fbxw7 合作调节辐射诱导的肿瘤发生。
Mol Cancer Res. 2012 Jun;10(6):834-44. doi: 10.1158/1541-7786.MCR-12-0025. Epub 2012 Apr 18.
4
LIMK2 is a crucial regulator and effector of Aurora-A-kinase-mediated malignancy.LIMK2 是 Aurora-A-激酶介导的恶性肿瘤的关键调节因子和效应物。
J Cell Sci. 2012 Mar 1;125(Pt 5):1204-16. doi: 10.1242/jcs.092304.
5
Targeting Aurora A kinase activity with the investigational agent alisertib increases the efficacy of cytarabine through a FOXO-dependent mechanism.以 Aurora A 激酶活性为靶点的研究药物alisertib 通过 FOXO 依赖性机制增加阿糖胞苷的疗效。
Int J Cancer. 2012 Dec 1;131(11):2693-703. doi: 10.1002/ijc.27579. Epub 2012 Jun 28.
6
IQGAP1 interacts with Aurora-A and enhances its stability and its role in cancer.IQGAP1 与 Aurora-A 相互作用，增强其稳定性及其在癌症中的作用。
Biochem Biophys Res Commun. 2012 Apr 27;421(1):64-9. doi: 10.1016/j.bbrc.2012.03.112. Epub 2012 Mar 29.
7
Cell division control by the Chromosomal Passenger Complex.染色体乘客复合物对细胞分裂的控制。
Exp Cell Res. 2012 Jul 15;318(12):1407-20. doi: 10.1016/j.yexcr.2012.03.015. Epub 2012 Mar 24.
8
Nucleophosmin/B23 activates Aurora A at the centrosome through phosphorylation of serine 89.核仁磷酸蛋白/B23 通过丝氨酸 89 的磷酸化作用激活中心体上的 Aurora A。
J Cell Biol. 2012 Apr 2;197(1):19-26. doi: 10.1083/jcb.201107134. Epub 2012 Mar 26.
9
Kaposi's sarcoma herpesvirus upregulates Aurora A expression to promote p53 phosphorylation and ubiquitylation.卡波氏肉瘤相关疱疹病毒上调 Aurora A 的表达以促进 p53 的磷酸化和泛素化。
PLoS Pathog. 2012;8(3):e1002566. doi: 10.1371/journal.ppat.1002566. Epub 2012 Mar 1.
10
Molecular characterization of neuroendocrine prostate cancer and identification of new drug targets.神经内分泌前列腺癌的分子特征分析与新药靶标的鉴定。
Cancer Discov. 2011 Nov;1(6):487-95. doi: 10.1158/2159-8290.CD-11-0130.

极光激酶 A（AURKA）在正常和病理细胞分裂中的作用。

Aurora A kinase (AURKA) in normal and pathological cell division.

机构信息

Program in Developmental Therapeutics, Fox Chase Cancer Center, W406, 333 Cottman Ave., Philadelphia, PA 19111, USA.

出版信息

Cell Mol Life Sci. 2013 Feb;70(4):661-87. doi: 10.1007/s00018-012-1073-7. Epub 2012 Aug 3.

DOI:10.1007/s00018-012-1073-7
PMID:22864622
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3607959/
Abstract

Temporally and spatially controlled activation of the Aurora A kinase (AURKA) regulates centrosome maturation, entry into mitosis, formation and function of the bipolar spindle, and cytokinesis. Genetic amplification and mRNA and protein overexpression of Aurora A are common in many types of solid tumor, and associated with aneuploidy, supernumerary centrosomes, defective mitotic spindles, and resistance to apoptosis. These properties have led Aurora A to be considered a high-value target for development of cancer therapeutics, with multiple agents currently in early-phase clinical trials. More recently, identification of additional, non-mitotic functions and means of activation of Aurora A during interphase neurite elongation and ciliary resorption have significantly expanded our understanding of its function, and may offer insights into the clinical performance of Aurora A inhibitors. Here we review the mitotic and non-mitotic functions of Aurora A, discuss Aurora A regulation in the context of protein structural information, and evaluate progress in understanding and inhibiting Aurora A in cancer.

摘要

时空调控 Aurora A 激酶（AURKA）的激活可调节中心体成熟、进入有丝分裂、形成和功能的双极纺锤体以及胞质分裂。Aurora A 的基因扩增和 mRNA 及蛋白过表达在许多类型的实体瘤中很常见，并与非整倍体、多余的中心体、有缺陷的有丝分裂纺锤体和抗凋亡有关。这些特性使得 Aurora A 被认为是癌症治疗药物开发的高价值靶点，目前有多种药物处于早期临床试验阶段。最近，在有丝分裂间期神经突伸长和纤毛吸收过程中发现了 Aurora A 的其他非有丝分裂功能和激活方式，这极大地扩展了我们对其功能的理解，并可能为 Aurora A 抑制剂的临床疗效提供线索。在这里，我们综述了 Aurora A 的有丝分裂和非有丝分裂功能，讨论了 Aurora A 在蛋白结构信息背景下的调控，并评估了在理解和抑制癌症中的 Aurora A 方面的进展。