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极光激酶B的过表达与甲状腺癌的未分化表型相关,并且是甲状腺癌细胞增殖所必需的。

Aurora B overexpression associates with the thyroid carcinoma undifferentiated phenotype and is required for thyroid carcinoma cell proliferation.

作者信息

Sorrentino Rosanna, Libertini Silvana, Pallante Pier Lorenzo, Troncone Giancarlo, Palombini Lucio, Bavetsias Vassilios, Spalletti-Cernia Daniela, Laccetti Paolo, Linardopoulos Spiros, Chieffi Paolo, Fusco Alfredo, Portella Giuseppe

机构信息

Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università Federico II, via S. Pansini 5, 80131 Napoli, Italy.

出版信息

J Clin Endocrinol Metab. 2005 Feb;90(2):928-35. doi: 10.1210/jc.2004-1518. Epub 2004 Nov 23.


DOI:10.1210/jc.2004-1518
PMID:15562011
Abstract

Alterations in chromosome number (aneuploidy) are common in human neoplasias. Loss of mitotic regulation is believed to induce aneuploidy in cancer cells and act as a driving force during the malignant progression. The serine/theronine protein kinases of aurora family genes play a critical role in the regulation of key cell cycle processes. Aurora B mediates chromosome segregation by ensuring orientation of sister chromatids and overexpression of Aurora B in diploid human cells NHDF (normal human diploid fibroblast) induces multinuclearity. We analyzed Aurora B expression in human thyroid carcinomas. Cell lines originating from different histotypes showed an increase in Aurora B expression. Immunohistochemical analysis of archive samples showed a high expression of Aurora B in anaplastic thyroid carcinomas; conversely, Aurora B expression was not detectable in normal thyroid tissue. Real-time PCR analysis confirmed a strong expression of Aurora B in anaplastic thyroid carcinomas. The block of Aurora B expression induced by RNA interference or by using an inhibitor of Aurora kinase activity significantly reduced the growth of thyroid anaplastic carcinoma cells.

摘要

染色体数目改变(非整倍体)在人类肿瘤中很常见。有丝分裂调控的丧失被认为会诱导癌细胞产生非整倍体,并在恶性进展过程中充当驱动力。极光激酶家族基因的丝氨酸/苏氨酸蛋白激酶在关键细胞周期进程的调控中起关键作用。极光B通过确保姐妹染色单体的定向来介导染色体分离,并且在二倍体人类细胞NHDF(正常人二倍体成纤维细胞)中极光B的过表达会诱导多核形成。我们分析了人类甲状腺癌中极光B的表达。源自不同组织类型的细胞系显示极光B表达增加。存档样本的免疫组织化学分析显示,未分化甲状腺癌中极光B表达较高;相反,在正常甲状腺组织中未检测到极光B表达。实时PCR分析证实未分化甲状腺癌中极光B有强烈表达。RNA干扰或使用极光激酶活性抑制剂诱导的极光B表达阻断显著降低了甲状腺未分化癌细胞的生长。

相似文献

[1]
Aurora B overexpression associates with the thyroid carcinoma undifferentiated phenotype and is required for thyroid carcinoma cell proliferation.

J Clin Endocrinol Metab. 2005-2

[2]
Expression of Aurora kinases in human thyroid carcinoma cell lines and tissues.

Int J Cancer. 2006-7-15

[3]
Aurora B expression directly correlates with prostate cancer malignancy and influence prostate cell proliferation.

Prostate. 2006-2-15

[4]
Transforming acidic coiled-coil 3 and Aurora-A interact in human thyrocytes and their expression is deregulated in thyroid cancer tissues.

Endocr Relat Cancer. 2007-9

[5]
Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype.

BMC Cancer. 2007-11-13

[6]
Aurora kinases are expressed in medullary thyroid carcinoma (MTC) and their inhibition suppresses in vitro growth and tumorigenicity of the MTC derived cell line TT.

BMC Cancer. 2011-9-26

[7]
Editorial: anaplastic carcinoma of the thyroid--will aurora B light a path for treatment?

J Clin Endocrinol Metab. 2005-2

[8]
Aurora A is differentially expressed and regulated in chromosomal and microsatellite instable sporadic colorectal cancers.

Mod Pathol. 2009-10

[9]
Gene amplification and overexpression of Aurora-C in breast and prostate cancer cell lines.

Oncol Res. 2012

[10]
Aurora kinases: new molecular targets in thyroid cancer therapy.

Clin Ter. 2012-11

引用本文的文献

[1]
Epigenetic control in thyroid cancer: mechanisms and clinical perspective.

Cell Death Discov. 2025-8-17

[2]
Rsk2 inhibition induces an aneuploid post-mitotic arrest of cell cycle progression in osteosarcoma cells.

Cell Death Discov. 2025-7-10

[3]
AURKB inhibition induces rhabdomyosarcoma apoptosis and ferroptosis through NPM1/SP1/ACSL5 axis.

JCI Insight. 2025-2-10

[4]
AURKB affects the proliferation of clear cell renal cell carcinoma by regulating fatty acid metabolism.

Discov Oncol. 2025-1-27

[5]
Centromeres in cancer: Unraveling the link between chromosomal instability and tumorigenesis.

Med Oncol. 2024-10-1

[6]
AURKB promotes bladder cancer progression by deregulating the p53 DNA damage response pathway via MAD2L2.

J Transl Med. 2024-3-21

[7]
The therapeutic potential of targeting the CHD protein family in cancer.

Pharmacol Ther. 2024-4

[8]
Construction of a hepatocytes-related and protein kinase-related gene signature in HCC based on ScRNA-Seq analysis and machine learning algorithm.

J Physiol Biochem. 2023-11

[9]
BI-847325, a selective dual MEK and Aurora kinases inhibitor, reduces aggressive behavior of anaplastic thyroid carcinoma on an in vitro three-dimensional culture.

Cancer Cell Int. 2022-12-8

[10]
Aurora Kinases as Therapeutic Targets in Head and Neck Cancer.

Cancer J.

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