Open AccessIGF 2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL 1
Author(s) -
Zhi Zhengke,
Zhu Hairong,
Lv Xiaofeng,
Lu Changgui,
Li Yang,
Wu Feng,
Zhou Lingling,
Li Hongxing,
Tang Weibing
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13756
Subject(s) - gene knockdown , gene silencing , cell growth , microrna , hirschsprung's disease , biology , rna interference , reporter gene , cancer research , microbiology and biotechnology , cell , hek 293 cells , cell migration , gene , disease , gene expression , rna , medicine , pathology , genetics
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 mi RNA s and their host genes in various disease, few was mentioned in HSCR although. In this study, miR‐483‐3p along with its host gene IGF 2 (Insulin‐like growth factor 2) was found down‐regulated in 60 HSCR aganglionic colon tissues compared with 60 normal controls. FHL 1 (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 ‐ SY 5Y cell lines by performing Transwell and CCK 8 assays. In conclusion, the knockdown of miR‐483‐3p and IGF 2 both suppressed cell migration and proliferation, while the loss of FHL 1 leads to opposite outcome. Furthermore, miR‐483‐3p mimics could rescue the negative effects on cell proliferation and migration caused by silencing IGF 2, while the FHL 1 si RNA may inverse the function of miR‐483‐3p inhibitor. This study revealed that miR‐483‐3p derived from IGF 2 was associated with Hirschsprung's disease by targeting FHL 1 and may provide a new pathway to understand the aetiology of HSCR .