ZYG11A serves as an oncogene in non-small cell lung cancer and influences CCNE1 expression

被引:25
作者
Wang, Xin [1 ,2 ]
Sun, Qi [3 ]
Chen, Chen [4 ]
Yin, Rong [1 ,5 ]
Huang, Xing [1 ,2 ]
Wang, Xuan [2 ]
Shi, Run [1 ,2 ]
Xu, Lin [1 ,5 ]
Ren, Binhui [1 ,5 ]
机构
[1] Canc Inst Jiangsu Prov, Dept Jiangsu Key Lab Mol & Translat Canc Res, Nanjing, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Clin Coll 4, Nanjing, Jiangsu, Peoples R China
[3] Southern Med Univ, Jinling Hosp, Dept Cardiothorac Surg, Nanjing, Jiangsu, Peoples R China
[4] Nanjing Med Univ, Dept Clin Coll 2, Nanjing, Jiangsu, Peoples R China
[5] Jiangsu Canc Hosp, Dept Thorac Surg, Nanjing, Jiangsu, Peoples R China
基金
美国国家科学基金会;
关键词
ZYG11A; CCNE1; NSCLC; Bioinformatics; Oncogene; OVER-EXPRESSION; CYCLIN-E; GENE; PROGNOSIS; ZYG-11; GROWTH; CUL-2; PITX2; ADENOCARCINOMA; METHYLATION;
D O I
10.18632/oncotarget.6904
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
By analyzing The Cancer Genome Atlas (TCGA) database, we identified ZYG11A as a potential oncogene. We determined the expression of ZYG11A in NSCLC tissues and explored its clinical significance. And also evaluated the effects of ZYG11A on NSCLC cell proliferation, migration, and invasion both in vitro and in vivo. Our results show that ZYG11A is hyper-expressed in NSCLC tissues compared to adjacent normal tissues, and increased expression of ZYG11A is associated with a poor prognosis (HR: 2.489, 95% CI: 1.248-4.963, p = 0.010). ZYG11A knockdown induces cell cycle arrest and inhibits proliferation, migration, and invasion of NSCLC cells. ZYG11A knockdown also results in decreased expression of CCNE1. Over-expression of CCNE1 in cells with ZYG11A knockdown restores their oncogenic activities. Our data suggest that ZYG11A may serve as a novel oncogene promoting tumorigenicity of NSCLC cells by inducing cell cycle alterations and increasing CCNE1 expression.
引用
收藏
页码:8029 / 8042
页数:14
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