Nidogen-1 is a common target of microRNAs MiR-192/215 in the pathogenesis of Hirschsprung's disease
Authors: Chao Xu
Hua Xie
Ankur Sharan
Peng Cai
Pingfa Chen
Hairong Zhu
Yankai Xia
Dongmei Zhu
Weibing Tang
Hongxing Li
Journal: Journal of Neurochemistry (2015)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: 3′-UTR; HSCR; gene regulation; microRNA; neural crest cell
Affiliations: Department of Pediatric Surgery, Nanjing Children Hospital Affiliated Nanjing Medical University, Nanjing, China., State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China., Key Laboratory of Modern Toxicology (Nanjing Medical University), Ministry of Education, China.

Abstract:  Recent studies have emphasized the important role of microRNA (miRNA) clusters and common target genes in disease progression. Despite the known involvement of the miR-192/215 family in many human diseases, its biological role in Hirschsprung disease (HSCR) remains undefined. In this study, we explored the role of the miR-192/215 family in the pathogenesis of HSCR. Quantitative real-time PCR and western blotting measured relative expression levels of miRNAs, mRNAs, and proteins in 80 HSCR patients and 77 normal colon tissues. Targets were evaluated by dual-luciferase reporter assays, and the functional effects of miR-192/215 on human 293T and SH-SY5Y cells were detected by the Transwell assay, CCK8 assay and flow cytometry. MiR-192/215 was significantly down-regulated in HSCR tissue samples, and their knockdown inhibited cell migration and proliferation in the human 293T and SH-SY5Y cell lines. Nidogen 1 (NID1) was confirmed as a common target gene of miR-192/215 by dual-luciferase reporter gene assay and its expression was inversely correlated with that of miR-192/215 in tissue samples and cell lines. Silencing of NID1 could rescue the extent of the suppressing effects by miR-192/215 inhibitor. The down-regulation of miR-192/215 may contribute to HSCR development by targeting NID1. We proposed the following cascade for the proposed mechanism of miR-192/215 in the pathogenesis of Hirschsprung disease (HSCR) by targeting Nidogen 1 (NID1). Aberrant expression of miR-192/215 inhibits cell migration and cell proliferation via NID1. We think the miR-192/miR-215/NID1 signaling pathway may play an important role in the pathogenesis of HSCR. 

Retracted: No

PubPeer comments:
 This article has a 2019 Correction, which reads:  The authors would like to correct some errors in the article u2018Nidogenu20101 is a common target of microRNAs MiRu2010192 215 in the pathogenesis of Hirschsprung s diseaseu2019 by Zhu et. al. (J. Neurochem., 134: 39u201346. https: doi.org 10.1111 jnc.13118). In Figs 1 and 3, the tranwell pictures of panel (b) and panel (a) are as follows: [FIGURE] [*sic*] Here are the original transwell images in Figures 1B and 3A, marked for noted duplications with boxes of the same color. ![file] Both sets of images were replaced by completely different images: ![file] , 
 #1 Thank you very much for your kindly comments. We have carefully checked and confirmed the accuracy of the data result, and published the correction. However, each set of experiments was repeated three times, and we used another set of images. we have reflected on it and standardized the image preservation mode of each experiment. Thanks again for your guidance. ,