Oncotarget

Research Papers:

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

Xin Wang _, Qi Sun, Chen Chen, Rong Yin, Xing Huang, Xuan Wang, Run Shi, Lin Xu and Binhui Ren

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Oncotarget. 2016; 7:8029-8042. https://doi.org/10.18632/oncotarget.6904

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Abstract

Xin Wang1,2, Qi Sun3, Chen Chen4, Rong Yin1,5, Xing Huang1,2, Xuan Wang2, Run Shi1,2, Lin Xu1,5, Binhui Ren1,5

1Department of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China

2Department of The Fourth Clinical College, Nanjing Medical University, Nanjing, Jiangsu, China

3Department of Cardiothoracic Surgery at Jinling Hospital, Southern Medical University, Nanjing, Jiangsu, China

4Department of The Second Clinical College, Nanjing Medical University, Nanjing, Jiangsu, China

5Department of Thoracic Surgery, Jiangsu Cancer Hospital, Nanjing, Jiangsu, China

Correspondence to:

Lin Xu, e-mail: xulin83cn@outlook.com

BinHui Ren, e-mail: robbishren@163.com

Keywords: ZYG11A, CCNE1, NSCLC, Bioinformatics, Oncogene

Received: September 21, 2015     Accepted: January 06, 2016     Published: January 12, 2016

ABSTRACT

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.


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