ArticleScientific reports2015
Down-regulation of miR-206 is associated with Hirschsprung disease and suppresses cell migration and proliferation in cell models.
Article in Scientific reports, 2015. 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 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- miR-146b-5p Regulates the Enteric Nervous System Development in Hirschsprung Disease via Targeting RET Pathway.Biochemical genetics · 2025Article
- The roles of non-coding RNAs in Hirschsprung's disease.Non-coding RNA research · 2024Review
- Bioinformatics Prediction for Network-Based Integrative Multi-Omics Expression Data Analysis in Hirschsprung Disease.Biomolecules · 2024Article
- 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
- Identifying the potential transcriptional regulatory network in Hirschsprung disease by integrated analysis of microarray datasets.World journal of pediatric surgery · 2023Article
- Emerging roles and mechanisms of miR-206 in human disorders: a comprehensive review.Cancer cell international · 2022Review
- Article
- Association betweenThe Journal of international medical research · 2020Article
- Increased miR-214 expression suppresses cell migration and proliferation in Hirschsprung disease by interacting with PLAGL2.Pediatric research · 2019Article
- Epigenetic Mechanisms in Hirschsprung Disease.International journal of molecular sciences · 2019Review
- Aberrant expressions of miRNA-206 target, FN1, in multifactorial Hirschsprung disease.Orphanet journal of rare diseases · 2019Article
- Activation of AMPK inhibits TGF-β1-induced airway smooth muscle cells proliferation and its potential mechanisms.Scientific reports · 2018Article
- Long non-coding RNA LOC100507600 functions as a competitive endogenous RNA to regulate BMI1 expression by sponging miR128-1-3p in Hirschsprung's disease.Cell cycle (Georgetown, Tex.) · 2018Article
- MicroRNA-939 inhibits cell proliferation via targeting LRSAM1 in Hirschsprung's disease.Aging · 2017Article
- Circular RNA ZNF609 functions as a competitive endogenous RNA to regulate AKT3 expression by sponging miR-150-5p in Hirschsprung's disease.Oncotarget · 2017Article
- Hirschsprung's disease: clinical dysmorphology, genes, micro-RNAs, and future perspectives.Pediatric research · 2017Review
- Mouse models of Hirschsprung disease and other developmental disorders of the enteric nervous system: Old and new players.Developmental biology · 2016Review
- Preischemic Administration of Nonexpanded Adipose Stromal Vascular Fraction Attenuates Acute Renal Ischemia/Reperfusion Injury and Fibrosis.Stem cells translational medicine · 2016Article
- Serum deprivation response inhibits breast cancer progression by blocking transforming growth factor-β signaling.Cancer science · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hirschsprung disease (HSCR) is a well-known congenital digestive disease that originates due to the developmental disorder of neural crest cells. MiR-206 is kown to have a relationship with digestive malfunctions. Therefore, we investigated whether or not miR-206 was involved in the pathogenesis of HSCR. qRT-PCR and Western blot assays were used to detect the expression levels of miRNA and mRNAs, and proteins in case and control tissue samples and two cell lines (293T and SH-SY5Y). The functions of miR-206 in vitro were measured by transwell assay, CCK8 assay and flow cytometry. Finally, we conducted dual-luciferase reporter assay to verify the connections between miR-206 and the target mRNA SDPR. Down-regulation of miR-206 was found in HSCR case tissue samples compared with controls, which was validated to be connected with the increased level of mRNA and protein of SDPR by qRT-PCR and dual-luciferase reporter assay. Moreover, miR-206 suppressed the cell migration and proliferation and silencing of SDPR could rescue the extent of the suppressing effects by miR-206 inhibitor. The findings suggest that miR-206 may play a significant role in the pathogenesis of HSCR, as well as inhibiting the cell migration and proliferation by targeting SDPR in disease models.
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