ZYG11A serves as an oncogene in non-small cell lung cancer and influences CCNE1 expression
Metrics: PDF 2102 views | HTML 2495 views | ?
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
Lin Xu, e-mail: email@example.com
BinHui Ren, e-mail: firstname.lastname@example.org
Keywords: ZYG11A, CCNE1, NSCLC, Bioinformatics, Oncogene
Received: September 21, 2015 Accepted: January 06, 2016 Published: January 12, 2016
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.