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癌症中的有丝分裂失败:极光激酶 B 及其在非整倍体形成中的潜在作用。

Mitotic failures in cancer: Aurora B kinase and its potential role in the development of aneuploidy.

机构信息

Department of Pathology, University of Debrecen, Nagyerdei krt. 98., 4032, Debrecen, Hungary.

出版信息

Pathol Oncol Res. 2012 Oct;18(4):761-9. doi: 10.1007/s12253-012-9534-8. Epub 2012 Jul 29.

DOI:10.1007/s12253-012-9534-8
PMID:22843098
Abstract

One of the basic requirements during the process of cell division is to maintain genetic integrity and ensure normal ploidy. The family of Aurora kinases, composed of Aurora A, B and C, takes a major role in the control of centrosome cycle, mitotic entry, chromosome condensation and coordination of chromosomal movements. Deregulation of kinase expression was described in a series of different malignancies which was also associated with aneuploidy. Recently, Aurora kinases gained significant interest as potential therapeutic targets in oncology. While there is increasing evidence about the activities of Aurora A kinase during cancer progression, data are controversial regarding the role of Aurora B. In this review the biology of Aurora kinases and its potential relation to cancer progression is discussed with special focus on functional changes and determination of Aurora B kinase.

摘要

细胞分裂过程中的基本要求之一是保持遗传完整性并确保正常的倍性。Aurora 激酶家族由 Aurora A、B 和 C 组成,在控制中心体周期、有丝分裂进入、染色体浓缩和染色体运动协调方面起着重要作用。激酶表达的失调在一系列不同的恶性肿瘤中被描述,并且与非整倍体有关。最近,Aurora 激酶作为肿瘤学中的潜在治疗靶点引起了广泛关注。虽然越来越多的证据表明 Aurora A 激酶在癌症进展中的活性,但关于 Aurora B 的作用的数据存在争议。在这篇综述中,讨论了 Aurora 激酶的生物学及其与癌症进展的潜在关系,特别关注功能变化和 Aurora B 激酶的测定。

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Mitotic failures in cancer: Aurora B kinase and its potential role in the development of aneuploidy.癌症中的有丝分裂失败:极光激酶 B 及其在非整倍体形成中的潜在作用。
Pathol Oncol Res. 2012 Oct;18(4):761-9. doi: 10.1007/s12253-012-9534-8. Epub 2012 Jul 29.
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Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype.极光激酶A/丝氨酸苏氨酸激酶15(Aurora-A/STK15)同时过表达和中心体扩增会在具有微卫星不稳定性(MIN)表型的肿瘤细胞中诱导染色体不稳定。
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Aurora-C and Aurora-B share phosphorylation and regulation of CENP-A and Borealin during mitosis.在有丝分裂过程中,极光激酶C(Aurora-C)和极光激酶B(Aurora-B)共同参与着丝粒蛋白A(CENP-A)和Borealin的磷酸化及调控。
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本文引用的文献

1
High chromosome number in hematological cancer cell lines is a negative predictor of response to the inhibition of Aurora B and C by GSK1070916.血液癌细胞系中的高染色体数是对 Aurora B 和 C 的抑制作用(GSK1070916)反应不良的负预测因子。
J Transl Med. 2011 Jul 15;9:110. doi: 10.1186/1479-5876-9-110.
2
Genetic disruption of aurora B uncovers an essential role for aurora C during early mammalian development.遗传破坏极光 B 揭示了极光 C 在早期哺乳动物发育过程中的重要作用。
Development. 2011 Jul;138(13):2661-72. doi: 10.1242/dev.066381. Epub 2011 May 25.
3
Mitotic kinases regulate MT-polymerizing/MT-bundling activity of DDA3.
组蛋白修饰及其在淋巴恶性肿瘤中的靶向治疗。
Int J Mol Sci. 2021 Dec 27;23(1):253. doi: 10.3390/ijms23010253.
4
Investigating Transcriptional Dynamics Changes and Time-Dependent Marker Gene Expression in the Early Period After Skeletal Muscle Injury in Rats.大鼠骨骼肌损伤后早期转录动力学变化及时间依赖性标记基因表达的研究
Front Genet. 2021 Jun 17;12:650874. doi: 10.3389/fgene.2021.650874. eCollection 2021.
5
An Aurora kinase inhibitor, AMG900, inhibits glioblastoma cell proliferation by disrupting mitotic progression.极光激酶抑制剂 AMG900 通过破坏有丝分裂进程来抑制神经胶质瘤细胞增殖。
Cancer Med. 2018 Nov;7(11):5589-5603. doi: 10.1002/cam4.1771. Epub 2018 Sep 17.
6
Mutant KRAS Status Is Associated with Increased KRAS Copy Number Imbalance: a Potential Mechanism of Molecular Heterogeneity.突变型KRAS状态与KRAS拷贝数失衡增加相关:分子异质性的一种潜在机制。
Pathol Oncol Res. 2017 Apr;23(2):417-423. doi: 10.1007/s12253-016-0126-x. Epub 2016 Oct 15.
7
Multipolar mitosis and aneuploidy after chrysotile treatment: a consequence of abscission failure and cytokinesis regression.温石棉处理后的多极有丝分裂和非整倍体:胞质分裂失败和胞质分裂倒退的结果
Oncotarget. 2016 Feb 23;7(8):8979-92. doi: 10.18632/oncotarget.6924.
8
AMG 900, a potent inhibitor of aurora kinases causes pharmacodynamic changes in p-Histone H3 immunoreactivity in human tumor xenografts and proliferating mouse tissues.AMG 900,一种极光激酶的强效抑制剂,可在人肿瘤异种移植模型及增殖中的小鼠组织中引起组蛋白H3磷酸化免疫反应性的药效学变化。
J Transl Med. 2014 Nov 4;12:307. doi: 10.1186/s12967-014-0307-x.
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EBNA3C-mediated regulation of aurora kinase B contributes to Epstein-Barr virus-induced B-cell proliferation through modulation of the activities of the retinoblastoma protein and apoptotic caspases.EBNA3C 介导的 Aurora 激酶 B 的调节通过调节视网膜母细胞瘤蛋白和凋亡半胱氨酸蛋白酶的活性促进 Epstein-Barr 病毒诱导的 B 细胞增殖。
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Aurora B kinase expression in laryngeal squamous cell carcinoma and its prognostic implications.喉鳞状细胞癌中 Aurora B 激酶的表达及其预后意义。
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Genes Dev. 2010 Oct 1;24(19):2169-79. doi: 10.1101/gad.1945310.
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Significance of Aurora B overexpression in hepatocellular carcinoma. Aurora B Overexpression in HCC.肝细胞癌中 Aurora B 过表达的意义。Aurora B 在 HCC 中的过表达。
BMC Cancer. 2010 Aug 28;10:461. doi: 10.1186/1471-2407-10-461.
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Cell. 2010 Aug 6;142(3):444-55. doi: 10.1016/j.cell.2010.06.039.