Oncotarget

Research Papers:

Downregulated pseudogene CTNNAP1 promote tumor growth in human cancer by downregulating its cognate gene CTNNA1 expression

Xiangjian Chen, Hua Zhu, Xiaoli Wu, Xuemeng Xie, Guanli Huang, Xiaoqun Xu, Shi Li and Chungen Xing _

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Oncotarget. 2016; 7:55518-55528. https://doi.org/10.18632/oncotarget.10833

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Abstract

Xiangjian Chen1,2, Hua Zhu3, Xiaoli Wu4, Xuemeng Xie2, Guanli Huang5, Xiaoqun Xu6, Shi Li7, Chungen Xing1

1Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China

2Department of General Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

3Department of Obstetrics and Gynecology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

4Department of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

5Department of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

6Operating Room, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

7Department of Urology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

Correspondence to:

Chungen Xing, email: xingcg@qq.com

Xiangjian Chen, email: wz1370666@126.com

Keywords: CRC, ceRNA, qRT-PCR, lncRNA, CCK-8

Received: March 27, 2016     Accepted: June 17, 2016     Published: July 25, 2016

ABSTRACT

Accumulating evidence indicates that deregulation of cancer-associated pseudogene is involved in the pathogenesis of cancer. In the study, we demonstrated that pseudogene CTNNAP1, for the CTNNA1 gene, was dysregulated in colorectal cancer and the degree of dysregulation was remarkably associated with tumor node metastasis (TNM) stage (P<0.05). The mechanistic experiments revealed that pseudogene CTNNAP1 played a pivotal role in the regulation of its cognate gene CTNNA1 by competition for microRNA-141. Moreover, gain-of-function approaches showed that overexpression of CTNNAP1 or CTNNA1 significantly inhibited cell proliferation and tumor growth in vitro and in vivo by inducing G0/G1 cell cycle arrest. Our findings add a new regulatory circuit via competing endogenous RNA (ceRNA) cross-talk between pseudogene CTNNAP1 and its cognate gene CTNNA1, and provide new insights into potential diagnostic biomarker for monitoring human colorectal cancer.


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