Overexpression of ZIC5 promotes proliferation in non-small cell lung cancer

被引:29
|
作者
Sun, Qi [1 ]
Shi, Run [2 ]
Wang, Xin [2 ]
Li, Demin [1 ]
Wu, Haiwei [3 ]
Ren, Binhui [2 ]
机构
[1] Southern Med Univ, Jinling Hosp, Dept Cardiothorac Surg, East Zhongshan Rd 305, Nanjing 210002, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Thorac Surg, Affiliated Canc Hosp, Jiangsu Key Lab Mol & Translat Canc Res,Canc Inst, Baiziting 42, Nanjing 210009, Peoples R China
[3] Nanjing Univ, Sch Clin Med, Jinling Hosp, Dept Cardiothorac Surg, East Zhongshan Rd 305, Nanjing 210002, Jiangsu, Peoples R China
关键词
ZIC5; Oncogene; NSCLC; Proliferation; CCNB1; CDK1; FAMILY; GENES; CYCLE; STATISTICS; EMBRYOS; CHINA;
D O I
10.1016/j.bbrc.2016.09.098
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
Background: Non-small cell lung cancer (NSCLC) has become the leading cause of cancer-related deaths. It is therefore urgent that we identify new molecular targets to help cure NSCLC patients. Here, we identified ZIC5 as a potential novel oncogene. Methods: We detected the expression of ZIC5 in tumor and normal tissues of NSCLC patients using quantitative real-time PCR and explored its clinical appearance. We then knocked down ZIC5 to observe changes in NSCLC cell proliferation and metastasis. Nude mouse xenograft models were established to measure ZIC5's function in vivo. Results: Our results revealed that ZIC5 was expressed at dramatically higher levels in NSCLC tumor tissues than in normal tissues. High levels of ZIC5 expression were associated with a higher primary tumor grade. ZIC5 expression was significantly inhibited by small interfering RNA. After silencing ZIC5, the metastatic capacity of NSCLC cells was clearly lower. Knocking down ZIC5 significantly inhibited the proliferation of NSCLC cells, causing the cell cycle to be arrested in G2 phase. Xenograft tumor models showed that knocking down ZIC5 also inhibited tumor growth in vivo. Q-PCR and western blot analysis revealed that ZIC5 expression was closely associated with CCNB1 and CDK1 complex expression, while other cell cycle-related genes showed no significant correlation with ZIC5. Conclusions: Our experiment show that ZIC5 is highly upregulated in NSCLC tumor tissues and suggest that ZIC5 may act as an oncogene by influencing CCNB1 and CDK1 complex expression. ZIC5 may therefore be a potential biomarker and therapeutic target for NSCLC patients. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:502 / 509
页数:8
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