Oncotarget · 2016 · 176 citations · 28 references
Life SciencesGeneticsMolecular BiologyGene ExpressionSignal TransductionTranscriptional RegulationMicrorna-mediated RegulationNoncoding Rna BiologyNoncoding Rna FunctionRna InterferenceCircular Messenger RnaCircular Rna FunctionCircular Rna RegulationCircular RnasCompetitive Endogenous Rna InteractionsCompetitive Endogenous Rna RegulationHirschsprung Disease GeneticsNoncoding Rna-mediated Effects
// Lei Peng 1, 3, * , Guanglin Chen 1, 3, * , Zhongxian Zhu 1, 3, * , Ziyang Shen 1, 3 , Chunxia Du 1, 3 , Rujin Zang 1, 3 , Yang Su 1, 3 , Hua Xie 1, 3 , Hongxing Li 1, 3 , Xiaoqun Xu 1, 3 , Yankai Xia 1, 2 , Weibing Tang 1, 3 1 State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing China 2 Key Laboratory of Modern Toxicology, Nanjing Medical University, Ministry of Education, China 3 Department of Pediatric Surgery, Children’s Hospital of Nanjing Medical University, Nanjing China * These authors contributed equally to this work Correspondence to: Weibing Tang, email: twbcn@163.com 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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