Oncotarget

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This article has been corrected. Correction in: Oncotarget. 2019; 10:3313-14.

Circular RNA ZNF609 functions as a competitive endogenous RNA to regulate AKT3 expression by sponging miR-150-5p in Hirschsprung’s disease

Lei Peng, Guanglin Chen, Zhongxian Zhu, Ziyang Shen, Chunxia Du, Rujin Zang, Yang Su, Hua Xie, Hongxing Li, Xiaoqun Xu, Yankai Xia and Weibing Tang _

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Oncotarget. 2017; 8:808-818. https://doi.org/10.18632/oncotarget.13656

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Abstract

Lei Peng1,3,*, Guanglin Chen1,3,*, Zhongxian Zhu1,3,*, Ziyang Shen1,3, Chunxia Du1,3, Rujin Zang1,3, Yang Su1,3, Hua Xie1,3, Hongxing Li1,3, Xiaoqun Xu1,3, Yankai Xia1,2, Weibing Tang1,3

1State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing China

2Key Laboratory of Modern Toxicology, Nanjing Medical University, Ministry of Education, China

3Department of Pediatric Surgery, Children’s Hospital of Nanjing Medical University, Nanjing China

*These authors contributed equally to this work

Correspondence to:

Weibing Tang, email: [email protected]

Keywords: hirschsprung disease, circular RNA (circRNA), competing endogenous RNAs (ceRNA), proliferation, migration

Received: June 03, 2016     Accepted: November 12, 2016     Published: November 26, 2016

ABSTRACT

Research over the past decade suggested critical roles for circular RNAs in the natural growth and disease progression. However, it remains poorly defined whether the circular RNAs participate in Hirschsprung disease (HSCR). Here, we reported that the cir-ZNF609 was down-regulated in HSCR compared with normal bowel tissues. Furthermore, suppression of cir-ZNF609 inhibited the proliferation and migration of cells. We screened out several putative cir-ZNF609 ceRNAs of which the AKT3 transcript was selected. Finally, RNA immunoprecipitation and luciferase reporter assays demonstrated that cir-ZNF609 may act as a sponge for miR-150-5p to modulate the expression of AKT3. In conclusion, these findings illustrated that cir-ZNF609 took part in the onset of HSCR through the crosstalk with AKT3 by competing for shared miR-150-5p.


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