Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line
Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line作者机构：State Key Laboratory of Molecular Oncology Cancer Institute Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China Institute of Radiation Medicine Chinese Academy of Medical Sciences and Peking Union Medical College Tianjin China
出 版 物：《Cell Research》 (细胞研究(英文版))
年 卷 期：2006年第16卷第4期
页 面：356-366页
核心收录：
学科分类：0710[理学-生物学] 0831[工学-生物医学工程（可授工学、理学、医学学位）] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种]
主 题：Aurora-A apoptosis caspase-3 PARP esophageal squamous cell carcinoma (ESCC) siRNA
摘 要：Aurora-A kinase,a serine/threonine protein kinase,is a potential *** and overexpression of Au-rora-A have been found in several types of human tumors,including esophageal squamous cell carcinoma(ESCC).It hasbeen demonstrated that cells overexpressing Aurora-A are more resistant to cisplatin-induced ***,themolecular mechanisms mediating these effects remain largely *** this report,we showed that overexpressionof Aurora-A through stable transfection of pEGFP-Aurora-A in human ESCC KYSE150 cells significantly promotedcell proliferation and inhibited cisplatin- or UV irradiation-induced *** of caspase-3 and poly(ADP-ribose)polymerase(PARP)in Aurora-A overexpressing cells were substantially reduced after cisplatin or UV ***,we found that silencing of endogenous Aurora-A kinase with siRNA substantially enhanced sensitivityto cisplatin- or UV-induced apoptosis in human ESCC EC9706 *** parallel,overexpression of Aurora-A potentlyupregulated the expression of ***,the knockdown of Bc1-2 by siRNA abrogated the Aurora-A s effect oninhibiting *** together,these data provide evidence that Aurora-A overexpression promoting cell proliferationand inhibiting apoptosis,suggesting a novel mechanism that is closely related to malignant phenotype and anti-cancerdrugs resistance of ESCC cells.
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