ArticleYonsei medical journal2019
MicroRNA-206 Reduces Osteosarcoma Cell Malignancy
Article in Yonsei medical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- DDTC-Cu(I) inhibits human osteosarcoma cells growth by repressing MET/PI3K/AKT signaling pathway.Scientific reports · 2025Article
- The role and research progress of the MET signalling pathway in targeted therapy for osteosarcoma.Oncology reviews · 2025Review
- Feasibility and barriers to rapid establishment of patient-derived primary osteosarcoma cell lines in clinical management.iScience · 2024Review
- Interaction of ncRNAs and the PI3K/AKT/mTOR pathway: Implications for osteosarcoma.Open life sciences · 2024Review
- Functional role of MicroRNA/PI3K/AKT axis in osteosarcoma.Frontiers in oncology · 2023Review
- Molecular mechanism of microRNAs regulating apoptosis in osteosarcoma.Molecular biology reports · 2022Review
- Extracellular vesicles from bone mesenchymal stem cells transport microRNA-206 into osteosarcoma cells and target NRSN2 to block the ERK1/2-Bcl-xL signaling pathway.European journal of histochemistry : EJH · 2022Article
- Circular RNA circANKIB1 promotes the progression of osteosarcoma by regulating miR-217/PAX3 axis.Journal of bone oncology · 2021Article
- Down-regulation of EDN1 gene expression by circulating miR-206 is associated with risk of preeclampsia.Medicine · 2020Article
- Overexpression of miR-206 in osteosarcoma and its associated molecular mechanisms as assessed through TCGA and GEO databases.Oncology letters · 2020Article
- MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020Review
- Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020Article
- Crosstalk Mechanisms Between HGF/c-Met Axis and ncRNAs in Malignancy.Frontiers in cell and developmental biology · 2020Review
- MicroRNA-761 targets FGFR1 to suppress the malignancy of osteosarcoma by deactivating PI3K/Akt pathway.OncoTargets and therapy · 2019Article
- Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study was undertaken to explore how miR-206 represses osteosarcoma (OS) development. MATERIALS AND
methodsExpression levels of miR-206, PAX3, and MET mRNA were explored in paired OS and adjacent tissue specimens. A patient-derived OS cell line was established. miR-206 overexpression and knockdown were achieved by lentiviral transduction. PAX3 and MET overexpression were achieved by plasmid transfection. Treatment with hepatocyte growth factor (HGF) was utilized to activate c-Met receptor. Associations between miR-206 and PAX3 or MET mRNA in OS cells were verified by AGO2-RNA immunoprecipitation assay and miRNA pulldown assay. OS cell malignancy was evaluated
resultsExpression levels of miR-206 were significantly decreased in OS tissue specimens, compared to adjacent counterparts, and were inversely correlated with expression of PAX3 and MET mRNA. miR-206 directly interacted with PAX3 and MET mRNA in OS cells. miR-206 overexpression significantly reduced PAX3 and MET gene expression in OS cells
conclusionmiR-206 reduces OS cell malignancy
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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.