ArticleOncoTargets and therapy2019
NRAS Contributes to Retinoblastoma Progression Through SNHG16/miR-183-5p/NRAS Regulatory Network.
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 3 papers.
What it found
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- microRNA-181a-5p impedes the proliferation, migration, and invasion of retinoblastoma cells by targeting the NRAS proto-oncogene.Clinics (Sao Paulo, Brazil) · 2022Article
- Computational Analysis of Deleterious SNPs inFrontiers in genetics · 2022Article
- A Review on the Role of Small Nucleolar RNA Host Gene 6 Long Non-coding RNAs in the Carcinogenic Processes.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe oncogene of wild type neuroblastoma RAS viral oncogene homolog (NRAS) has been found to involve in the tumorigenesis of cancers. However, the role of NRAS in retinoblastoma (RB) progression remains largely unknown.
methodsThe expression levels of NRAS, miR-183-5p and small nucleolar RNA host gene 16 (SNHG16) were measured using quantitative real-time polymerase chain reaction assay or Western blot assay, respectively. Cell proliferation and apoptosis were analyzed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay or flow cytometry, respectively. Transwell assay was used to determine cell migration and invasion abilities. The interaction between miR-183-5p and NRAS or SNHG16 was analyzed using bioinformatics analysis and dual-luciferase reporter assay.
resultsNRAS was elevated in RB tissues and cell lines, knockdown of NRAS could inhibit proliferation, migration and invasion but induced apoptosis in vitro and suppressed tumor growth in vivo. NRAS was confirmed to be a target of miR-183-5p and was negatively regulated by miR-183-5p in RB cells. Moreover, overexpressed NRAS reversed miR-183-5p mediated inhibition on RB cell progression. Besides that, SNHG16 directly interacted with miR-183-5p and reduced miR-183-5p expression in RB cells. The suppression of RB cell progression induced by SNHG16 silencing could be partially attenuated by the inhibition of miR-183-5p. Besides that, SNHG16 could regulate NRAS expression through competitively binding to miR-183-5p in RB cells.
conclusionNRAS functioned as an oncogene to contribute to RB progression by SNHG16/miR-183-5p/NRAS regulatory network, indicating a novel and promising therapeutic target for RB.
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