AURKA promotes cancer metastasis by regulating epithelial-mesenchymal transition and cancer stem cell properties in hepatocellular carcinoma

被引:100
|
作者
Chen, Chenlin [1 ]
Song, Guangyuan [1 ]
Xiang, Jue [1 ]
Zhang, Hongcheng [1 ]
Zhao, Shaoyun [1 ]
Zhan, Yinchu [2 ]
机构
[1] Zhejiang Chinese Med Univ, Clin Med Coll 2, Hangzhou 310005, Zhejiang, Peoples R China
[2] Zhejiang Univ, Dept Hepatopancreatobiliary Surg, Int Hosp, 848 DongXinRd, Hangzhou 310000, Zhejiang, Peoples R China
关键词
AURKA; Radiation; Epithelial-mesenchymal transition (EMT); Cancer stem cell (CSC); Hepatocellular carcinoma; AURORA-KINASE; DEFINITIVE RADIOTHERAPY; TREATMENT RESISTANCE; TUMOR-GROWTH; RISK-FACTORS; RECURRENCE; PROGRESSION; SURVIVAL; INVASION; LINKS;
D O I
10.1016/j.bbrc.2017.03.075
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
AURKA (aurora kinase A) has been confirmed as an oncogene in cancer development; however, its role and underlying mechanisms in the metastasis of hepatocellular carcinoma (HCC) remain unknown. In this study, We found that AURKA was up-regulated in HCC tissues and correlated with pathological stage and distant metastasis. Further found that AURKA was involved in the cancer metastases after radiation in HCC. While overexpression of AURKA induced epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) behaviors though PI3K/AKT pathway, silencing AURKA suppressed radiation-enhanced cell invasiveness of HCC. Taken together, our results suggested that AURKA contributed in metastasis of irradiated residul HCC though facilitating EMT and CSC properties, suggesting the potential clinical application of AURKA inhibitors in radiotherapy for patients with HCC. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码:514 / 520
页数:7
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