Research Papers:
Downregulated pseudogene CTNNAP1 promote tumor growth in human cancer by downregulating its cognate gene CTNNA1 expression
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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: [email protected]
Xiangjian Chen, email: [email protected]
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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