ArticleInternational journal of molecular medicine2018
MicroRNA-139-5p/Flt1/Wnt/β-catenin regulatory crosstalk modulates the progression of glioma.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Non-coding RNAs-based Therapy and Angiogenesis: A New Era for the Management of Gliomas.Current gene therapy · 2026Review
- Integrating the secretome and interactome to identify novel biomarkers and therapeutic targets in colorectal cancer.Cell communication and signaling : CCS · 2025Article
- Evaluating glioblastoma tumour sphere growth and migration in interaction with astrocytes using 3D collagen-hyaluronic acid hydrogels.Journal of materials chemistry. B · 2023Article
- Review
- Roles of Non-coding RNAs and Angiogenesis in Glioblastoma.Frontiers in cell and developmental biology · 2021Review
- Vascular mimicry: changing the therapeutic paradigms in cancer.Molecular biology reports · 2020Review
- The Smad2/3/4 complex binds miR-139 promoter to modulate TGFβ-induced proliferation and activation of human Tenon's capsule fibroblasts through the Wnt pathway.Journal of cellular physiology · 2019Article
- Leptin-Induced Angiogenesis of EA.Hy926 Endothelial CellsFrontiers in pharmacology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fms-related tyrosine kinase 1 (Flt1), the receptor of VEGF/PIGF, is associated with cancer angiogenesis and tumorigenesis. Although the high expression of Flt1 in glioma is identified, its regulatory mechanism remains unclear. In the present study, we demonstrate that miR‑139‑5p inhibits Flt1 expression mediated by binding its 3' untranslated region (3'UTR) to regulate the progression of human glioma. We found miR‑139‑5p was downregulated in glioma tissues compared with normal brain tissues whereas a converse expression level of Flt1 was observed. Additionally we proved that miR‑139‑5p directly integrated with the 3'UTR of Flt1 via luciferase activity assay and cells transfected with miR‑139‑5p characterized with a low expression of Flt1 in mRNA and protein levels. Furthermore, we validated that miR‑139‑5p enforced its biological modulation via targeting Flt1 through rescue experiments. miR‑139‑5p suppressed and Flt1 stimulated the malignant activities of glioma cells. We demonstrated that miR‑139‑5p inhibited the Flt1-mediated Wnt/β-catenin signaling pathway in glioma cells. Conclusively, our study indicated that miR‑139‑5p can counteract the malignant phenotypes of glioma cells by the inhibitory effect of the Flt1-mediated Wnt/β-catenin signaling pathway.
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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.