Wang Xin, Sun Qi, Chen Chen, Yin Rong, Huang Xing, Wang Xuan, Shi Run, Xu Lin, Ren Binhui
Department of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.
Department of The Fourth Clinical College, Nanjing Medical University, Nanjing, Jiangsu, China.
Oncotarget. 2016 Feb 16;7(7):8029-42. doi: 10.18632/oncotarget.6904.
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.
通过分析癌症基因组图谱（TCGA）数据库，我们确定ZYG11A为一种潜在的致癌基因。我们测定了ZYG11A在非小细胞肺癌（NSCLC）组织中的表达，并探讨了其临床意义。此外，我们还评估了ZYG11A在体外和体内对NSCLC细胞增殖、迁移和侵袭的影响。我们的结果表明，与相邻正常组织相比，ZYG11A在NSCLC组织中高表达，且ZYG11A表达增加与预后不良相关（风险比：2.489，95%置信区间：1.248 - 4.963，p = 0.010）。敲低ZYG11A可诱导细胞周期停滞，并抑制NSCLC细胞的增殖、迁移和侵袭。敲低ZYG11A还导致细胞周期蛋白E1（CCNE1）表达降低。在敲低ZYG11A的细胞中过表达CCNE1可恢复其致癌活性。我们的数据表明，ZYG11A可能作为一种新型致癌基因，通过诱导细胞周期改变和增加CCNE1表达来促进NSCLC细胞的致瘤性。
