ArticleExperimental and therapeutic medicine2021
Long non-coding RNA small nucleolar RNA host gene 1 knockdown suppresses the proliferation, migration and invasion of osteosarcoma cells by regulating microRNA-424-5p/FGF2
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 6 citations in OpenAlex.
- LncSNHGs: new targets in osteosarcoma.Cancer gene therapy · 2025Review
- METTL3-mediated SNHG1 mFrontiers in oncology · 2025Article
- Osteosarcoma in a ceRNET perspective.Journal of biomedical science · 2024Review
- Role of miR-424 in the carcinogenesis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- LncRNA SNHG1: role in tumorigenesis of multiple human cancers.Cancer cell international · 2023Review
- N6-methyladenosine Modification-Related Long Non-Coding RNAs are Potential Biomarkers for Predicting the Prognosis of Patients With Osteosarcoma.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to clarify the effect of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on the proliferation, migration and invasion of osteosarcoma (OS) cells and to explore the potential underlying mechanisms. The expression levels of SNHG1, microRNA (miR)-424-5p and fibroblast growth factor 2 (FGF2) in OS tissues and cells were detected using reverse transcription-quantitative polymerase chain reaction. OS cell proliferation, migration and invasion were analysed by MTT, wound healing and Transwell invasion assays, respectively. The targeting relationships between SNHG1 and miR-424-5p, as well as between miR-424-5p and FGF2, were confirmed using RNA-binding protein immunoprecipitation and/or dual-luciferase reporter gene assays. The results demonstrated that the expression levels of SNHG1 and FGF2 were upregulated, whereas the expression of miR-424-5p was downregulated in OS tissues and cells. The silencing of SNHG1 significantly inhibited the proliferation, migration and invasion of OS cells. Additionally, FGF2 was shown to be a target of miR-424-5p, which in turn, was a target of SNHG1. miR-424-5p silencing and FGF2 overexpression both reversed the suppressive effects of SNHG1 knockdown on the proliferation, migration and invasion of OS cells. Thus, the silencing of SNHG1 may inhibit the proliferation, migration and invasion of OS cells by regulating the miR-424-5p/FGF2 axis.
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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 Socratic graph.