ArticleJournal of cellular and molecular medicine2018
IGF2-derived miR-483-3p associated with Hirschsprung's disease by targeting FHL1.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Integrative Regulatory Networks of MicroRNA-483: Unveiling Its Systematic Role in Human Diseases and Clinical Implications.Biomolecules · 2025Review
- MicroRNA regulation of enteric nervous system development and disease.Trends in neurosciences · 2025Review
- The roles of non-coding RNAs in Hirschsprung's disease.Non-coding RNA research · 2024Review
- Sequencing Reveals miRNAs Enriched in the Developing Mouse Enteric Nervous System.Non-coding RNA · 2023Article
- Pathogenic roles of microRNAs and competing endogenous RNAs in Hirschsprung disease (HSCR): Potential diagnostic markers for HSCR.Pediatric discovery · 2023Review
- Downregulation of miR-144 blocked the proliferation and invasion of nerve cells in Hirschsprung disease by regulating Transcription Factor AP 4 (TFAP4).Pediatric surgery international · 2023Article
- The abnormal phosphorylation of the Rac1, Lim-kinase 1, and Cofilin proteins in the pathogenesis of Hirschsprung's disease.Bioengineered · 2022Article
- LncRNA-RMST Functions as a Transcriptional Co-regulator of SOX2 to Regulate miR-1251 in the Progression of Hirschsprung's Disease.Frontiers in pediatrics · 2022Article
- Article
- Epigenetic Mechanisms in Hirschsprung Disease.International journal of molecular sciences · 2019Review
- Corrigendum.Journal of cellular and molecular medicine · 2019Article
- IGF2-derived miR-483-3p associated with Hirschsprung's disease by targeting FHL1.Journal of cellular and molecular medicine · 2018Article
Corrections and comments
- Erratum issuedCorrigendum.2019
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.