Sharan, Ankur
Zhu, Hairong
Xie, Hua
Li, Hongxing
Tang, Junwei
Tang, Weibing
Zhang, Hongwei
Xia, Yankai
Article History
Received: 21 August 2014
Accepted: 25 February 2015
First Online: 20 March 2015
Change Date: 6 January 2016
Change Type: Update
Change Details: A correction has been published and is appended to both the HTML and PDF versions of this paper. The error has not been fixed in the paper.
Change Date: 6 January 2016
Change Type: Erratum
Change Details: Hirschsprung disease (HSCR) is a well-known congenital digestive disease that originates due to the developmental disorder of neural crest cells. MiR-206 is kown to have a relationship with digestive malfunctions. Therefore, we investigated whether or not miR-206 was involved in the pathogenesis of HSCR. qRT-PCR and Western blot assays were used to detect the expression levels of miRNA and mRNAs, and proteins in case and control tissue samples and two cell lines (293T and SH-SY5Y). The functions of miR-206 <i>in vitro</i> were measured by transwell assay, CCK8 assay and flow cytometry. Finally, we conducted dual-luciferase reporter assay to verify the connections between miR-206 and the target mRNA <i>SDPR</i>. Down-regulation of miR-206 was found in HSCR case tissue samples compared with controls, which was validated to be connected with the increased level of mRNA and protein of <i>SDPR</i> by qRT-PCR and dual-luciferase reporter assay. Moreover, miR-206 suppressed the cell migration and proliferation and silencing of <i>SDPR</i> could rescue the extent of the suppressing effects by miR-206 inhibitor. The findings suggest that miR-206 may play a significant role in the pathogenesis of HSCR, as well as inhibiting the cell migration and proliferation by targeting <i>SDPR</i> in disease models.
Competing interests
: The authors declare no competing financial interests.