Oncotarget

Research Papers:

Nek7 is overexpressed in hepatocellular carcinoma and promotes hepatocellular carcinoma cell proliferation in vitro and in vivo

Lei Zhou, Zhixin Wang, Xinsen Xu, Yong Wan, Kai Qu, Haining Fan, Qiangpu Chen, Xuejun Sun and Chang Liu _

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Oncotarget. 2016; 7:18620-18630. https://doi.org/10.18632/oncotarget.7620

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Abstract

Lei Zhou1,2,3, Zhixin Wang2,4, Xinsen Xu2, Yong Wan2, Kai Qu2, Haining Fan4, Qiangpu Chen1, Xuejun Sun3, Chang Liu2

1Department of Hepatobiliary Surgery, The Affiliated Hospital of Binzhou Medical University, Binzhou, China

2Department of Hepatobiliary Surgery, The First Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, China

3Department of General Surgery, The First Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, China

4Department of Hepatopancreatobiliary Surgery, The Affiliated Hospital of Qinghai University, Xining, China

Correspondence to:

Qiangpu Chen, e-mail: [email protected]

Xuejun Sun, e-mail: [email protected]

Chang Liu, e-mail: [email protected]

Keywords: Nek7, hepatocellular carcinoma, cell proliferation, cyclin B1, prognosis

Received: October 20, 2015     Accepted: January 24, 2016     Published: February 23, 2016

ABSTRACT

NIMA-related kinase-7 (Nek7) is a serine/threonine kinase involved in cell-cycle progression via mitotic spindle formation and cytokinesis. In this study, we investigated whether Nek7 involves in hepatocellular carcinoma (HCC). Interestingly, we found that Nek7 was significantly overexpressed in HCC than in liver tissues. In HCC patients, high Nek7 expression was significantly correlated with tumor numbers, tumor diameter, adjacent organs invasion, tumor grade and TNM stage. Furthermore, Nek7 expression pattern showed close relationship with that of Ki-67, a well-stablished cell proliferation marker. More importantly, patients with higher expression levels of Nek7 had significantly lower 5-years survival rate. Likewise, Nek7 expression was significantly higher in HCC cell lines than normal hepatic cell line. By Nek7 silencing using lentivirus-mediated Nek7 interference approach, the growth of HCC cell lines was inhibited and the tumor growth in xenograft mouse model was also suppressed. Mechanistic studies showed that silencing of Nek7 resulted in decreasing cyclinB1 level both in vitro and in vivo. In conclusion, this study highlights for the first time the possible role of Nek7 in HCC progression. Nek7 would be a useful biomarker that early predicts HCC patients at higher risk of poor prognosis. Also, Nek7 could be a novel HCC therapeutic target.


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