ArticleCancer biomarkers : section A of Disease markers2019
MicroRNA-539 inhibits the progression of Wilms' Tumor through downregulation of JAG1 and Notch1/3.
Article in Cancer biomarkers : section A of Disease markers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Conservation of Epithelial-to-Mesenchymal Transition Process in Neural Crest Cells and Metastatic Cancer.Cells, tissues, organs · 2021Pooled it
- RNA‑binding protein DAZAP1 promotes gastric cancer metastasis by enhancing NOTCH1 and JAG1 mRNA stability.International journal of oncology · 2026Article
- Notch 3 regulates ferroptosis of lens epithelial cells in age-related cataract by PI3K/AKT pathway.Indian journal of ophthalmology · 2026Article
- Article
- MicroRNAs in kidney development and disease.JCI insight · 2022Review
- Differential expression of miRNA in histological subtype of Wilms tumor.Pediatric surgery international · 2022Article
- MiR-139-5p Inhibits the Development of Gastric Cancer through Targeting TPD52.Journal of healthcare engineering · 2022Article
- The effect of miR-539 regulating TRIAP1 on the apoptosis, proliferation, migration and invasion of osteosarcoma cells.Cancer cell international · 2021Article
- The anti-tumor effect of miR-539-3p on colon cancer via regulating cell viability, motility, and nude mouse tumorigenicity with CDK14 inhibition.Journal of gastrointestinal oncology · 2020Article
- Comprehensive analysis of the long non-coding RNA-associated competitive endogenous RNA network reveals novel prognostic biomarkers in Wilms' tumor.Oncology letters · 2020Article
- RNA-Sequencing, Connectivity Mapping, and Molecular Docking to Investigate Ligand-Protein Binding for Potential Drug Candidates for the Treatment of Wilms Tumor.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- [Expression of miR-155-5p in Wilms tumor and its regulatory role in proliferation, migration and apoptosis of Wilms tumor cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- A "NOTCH" Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer.Genes · 2019Review
- Downregulation miR-539 is associated with poor prognosis of gastric cancer patients and aggressive progression of gastric cancer cells.Cancer biomarkers : section A of Disease markers · 2019Article
- MicroRNA-215-5p Inhibits the Proliferation and Migration of Wilm's Tumor Cells by Targeting CRK.Technology in cancer research & treatmentArticle
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies demonstrated that miR-539 play an important role in the carcinogenesis of some cancers. The aim of the present study was to determine the role of miR-539 in the pathogenesis of Wilms' Tumor (WT).
methodsThe expression level of miR-539 was measured by qRT-PCR in 42 WT tissues and SK-NEP-1 cell line. Protein expression of genes (E-cadherin, N-cadherin, Vimentin, Notch 1, Notch 3 and JAG1) was assessed by Western blot. The function of miR-539 was investigated in SK-NEP-1 cells by MTT and Transwell assays. The relationship between miR-539 and JAG1 was verified by a dual luciferase assay in SK-NEP-1 cells.
resultsThe expression level of miR-539 was significantly decreased in WT tissues. Downregulation of miR-539 was closely related to NWTS-5 stage, lymph node metastasis and histological type of WT patients. Furthermore, low miR-539 expression was associated with a shorter overall survival rate in WT patients. In vitro, overexpression of miR-539 suppressed proliferation, migration and invasion of SK-NEP-1 cells. In addition, JAG1 was a direct target of miR-539. MiR-539 inhibited the development of WT by inhibiting JAG1-Notch1/3 expressing and blocking EMT.
conclusionMiR-539 inhibited the progression of WT through downregulation of JAG1 and Notch1/3.
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