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IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1

HSCR (Hirschsprung's disease) is a serious congenital defect, and the aetiology of it remains unclear. Many studies have highlighted the significant roles of intronic miRNAs and their host genes in various disease, few was mentioned in HSCR although. In this study, miR‐483‐3p along with its hos...

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Autores principales: Zhi, Zhengke, Zhu, Hairong, Lv, Xiaofeng, Lu, Changgui, Li, Yang, Wu, Feng, Zhou, Lingling, Li, Hongxing, Tang, Weibing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156468/
https://www.ncbi.nlm.nih.gov/pubmed/30073757
http://dx.doi.org/10.1111/jcmm.13756
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author Zhi, Zhengke
Zhu, Hairong
Lv, Xiaofeng
Lu, Changgui
Li, Yang
Wu, Feng
Zhou, Lingling
Li, Hongxing
Tang, Weibing
author_facet Zhi, Zhengke
Zhu, Hairong
Lv, Xiaofeng
Lu, Changgui
Li, Yang
Wu, Feng
Zhou, Lingling
Li, Hongxing
Tang, Weibing
author_sort Zhi, Zhengke
collection PubMed
description HSCR (Hirschsprung's disease) is a serious congenital defect, and the aetiology of it remains unclear. Many studies have highlighted the significant roles of intronic miRNAs and their host genes in various disease, few was mentioned in HSCR although. In this study, miR‐483‐3p along with its host gene IGF2 (Insulin‐like growth factor 2) was found down‐regulated in 60 HSCR aganglionic colon tissues compared with 60 normal controls. FHL1 (Four and a half LIM domains 1) was determined as a target gene of miR‐483‐3p via dual‐luciferase reporter assay, and its expression was at a higher level in HSCR tissues. Here, we study cell migration and proliferation in human 293T and SH‐SY5Y cell lines by performing Transwell and CCK8 assays. In conclusion, the knockdown of miR‐483‐3p and IGF2 both suppressed cell migration and proliferation, while the loss of FHL1 leads to opposite outcome. Furthermore, miR‐483‐3p mimics could rescue the negative effects on cell proliferation and migration caused by silencing IGF2, while the FHL1 siRNA may inverse the function of miR‐483‐3p inhibitor. This study revealed that miR‐483‐3p derived from IGF2 was associated with Hirschsprung's disease by targeting FHL1 and may provide a new pathway to understand the aetiology of HSCR.
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spelling pubmed-61564682018-10-01 IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1 Zhi, Zhengke Zhu, Hairong Lv, Xiaofeng Lu, Changgui Li, Yang Wu, Feng Zhou, Lingling Li, Hongxing Tang, Weibing J Cell Mol Med Original Articles HSCR (Hirschsprung's disease) is a serious congenital defect, and the aetiology of it remains unclear. Many studies have highlighted the significant roles of intronic miRNAs and their host genes in various disease, few was mentioned in HSCR although. In this study, miR‐483‐3p along with its host gene IGF2 (Insulin‐like growth factor 2) was found down‐regulated in 60 HSCR aganglionic colon tissues compared with 60 normal controls. FHL1 (Four and a half LIM domains 1) was determined as a target gene of miR‐483‐3p via dual‐luciferase reporter assay, and its expression was at a higher level in HSCR tissues. Here, we study cell migration and proliferation in human 293T and SH‐SY5Y cell lines by performing Transwell and CCK8 assays. In conclusion, the knockdown of miR‐483‐3p and IGF2 both suppressed cell migration and proliferation, while the loss of FHL1 leads to opposite outcome. Furthermore, miR‐483‐3p mimics could rescue the negative effects on cell proliferation and migration caused by silencing IGF2, while the FHL1 siRNA may inverse the function of miR‐483‐3p inhibitor. This study revealed that miR‐483‐3p derived from IGF2 was associated with Hirschsprung's disease by targeting FHL1 and may provide a new pathway to understand the aetiology of HSCR. John Wiley and Sons Inc. 2018-08-02 2018-10 /pmc/articles/PMC6156468/ /pubmed/30073757 http://dx.doi.org/10.1111/jcmm.13756 Text en © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Zhi, Zhengke
Zhu, Hairong
Lv, Xiaofeng
Lu, Changgui
Li, Yang
Wu, Feng
Zhou, Lingling
Li, Hongxing
Tang, Weibing
IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1
title IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1
title_full IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1
title_fullStr IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1
title_full_unstemmed IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1
title_short IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1
title_sort igf2‐derived mir‐483‐3p associated with hirschsprung's disease by targeting fhl1
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156468/
https://www.ncbi.nlm.nih.gov/pubmed/30073757
http://dx.doi.org/10.1111/jcmm.13756
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