ArticleOncoTargets and therapy2019
Upregulation Of miR-149-3p Suppresses Spinal Chordoma Malignancy By Targeting Smad3.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- miR-149-3p targetingBiomolecules & biomedicine · 2024Article
- DDX17 induces epithelial-mesenchymal transition and metastasis through the miR-149-3p/CYBRD1 pathway in colorectal cancer.Cell death & disease · 2023Article
- Article
- Impacts of MicroRNAs Induced by the Gut Microbiome on Regulating the Development of Colorectal Cancer.Frontiers in cellular and infection microbiology · 2022Review
- Large Scale Molecular Studies of Pituitary Neuroendocrine Tumors: Novel Markers, Mechanisms and Translational Perspectives.Cancers · 2021Review
- LINC00472 regulates vascular smooth muscle cell migration and proliferation via regulating miR-149-3p.Environmental science and pollution research international · 2021Article
- LncRNA NONHSAT114552 Sponges miR-320d to Promote Proliferation and Invasion of Chordoma Through Upregulating NRP1.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeDysregulation of miRNAs plays an important role in the malignancy of different tumors including chordoma. Expression of miR-149-3p was earlier reported to be downregulated in chordoma tissue. However, its biological role remains to be unrevealed in chordoma, especially in spinal chordoma.
methodsExpression of miR-149-3p and Smad3 was detected by RT-qPCR and Western blot. Chordoma malignancy was evaluated by cell proliferation, migration, invasion, and apoptosis using MTT assay, transwell assay, flow cytometry analyzing apoptosis rate, and Western blot-determined expression of Bcl-2, Bax, and cleaved caspase 3, respectively. The target binding between miR-149-3p and Smad3 was predicted by TargetScan Human website and confirmed by luciferase reporter assay and RNA immunoprecipitation. Xenograft tumors were generated, and expression of miR-149-3p and Smad3 was investigated in vivo.
resultsmiR-149-3p was downregulated in spinal chordoma tissues and cells, and its overexpression promoted chordoma cell apoptosis and inhibited proliferation, migration, and invasion in U-CH1 and MUG-Chor1 cells. Unexpectedly, Smad3 was a downstream target of miR-149-3p and negatively correlated with miR-149-3p expression in chordoma tissues. Besides, Smad3 was upregulated in chordoma tissues and its silencing had a similar effect as miR-149-3p overexpression in U-CH1 and MUG-Chor1 cells. Moreover, Smad3 upregulation could partially reverse the tumor-suppressive effect of miR-149-3p in chordoma cells. In vivo, the tumorigenesis of U-CH1 and MUG-Chor1 cells was impaired by upregulated miR-149-3p through decreasing Smad3 expression.
conclusionmiR-149-3p could serve as a tumor suppressor in spinal chordoma through targeting and downregulating Smad3.
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