Oncotarget

Research Papers:

This article has been corrected. Correction in: Oncotarget. 2019; 10:4501-4502.

Downregulation of lncRNA MEG3 and miR-770-5p inhibit cell migration and proliferation in Hirschsprung’s disease

Hongxing Li, Bo Li, Dongmei Zhu, Hua Xie, Chunxia Du, Yankai Xia and Weibing Tang _

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Oncotarget. 2017; 8:69722-69730. https://doi.org/10.18632/oncotarget.19207

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Abstract

Hongxing Li1,2,*, Bo Li1,2,*, Dongmei Zhu2,4,*, Hua Xie1,2, Chunxia Du1,2, Yankai Xia2,3 and Weibing Tang1,2,*

1Department of Pediatric Surgery, Children’s Hospital of Nanjing Medical University, Nanjing, China

2State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China

3Key Laboratory of Modern Toxicology, Nanjing Medical University, Ministry of Education, Nanjing, China

4Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Nantong University, Nantong, China

*These authors have contributed equally to this work

Correspondence to:

Weibing Tang, email: twbcn@njmu.edu.cn

Keywords: lncRNA, miRNA, gene regulation, Hirschsprung’s disease

Received: December 15, 2016     Accepted: June 10, 2017     Published: July 12, 2017

ABSTRACT

The long noncoding RNA (lncRNA) MEG3 is involved in various biological processes including cell migration and cell proliferation. In present study, it was found that MEG3 and the intronic miR-770-5p were decreased in samples from HSCR patients. Besides, knockdown of MEG3 and miR-770-5p suppressed cell migration and proliferation, while cell cycle and apoptosis were not affected in human 293T and SH-SY5Y cells. SRGAP1 mRNA and protein upregulation was inversely correlated with miR-770-5p expression in tissue samples and cell lines, which was confirmed to be a target gene of miR-770-5p by dual-luciferase reporter assay. Moreover, silencing of SRGAP1 rescued the inhibition of cell migration and proliferation induced by MEG3 siRNA and miR-770-5p inhibition. The present study elucidates a novel mechanism of the development of HSCR and shows that the MEG3/miR-770-5p/SRGAP1 pathway plays a vital role in the pathogenesis of HSCR.


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