ArticleOncoTargets and therapy2019
Long Noncoding RNA SNHG16 Sponges miR-182-5p And miR-128-3p To Promote Retinoblastoma Cell Migration And Invasion By Targeting LASP1.
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 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Diverse functional roles of miR-128-3p in human diseases: Focus on its roles in human cancer.Genes & diseases · 2026Review
- MicroRNAs' Significance in Retinoblastoma Diagnosis and Treatment: The Little Heroes.Biochemical genetics · 2025Review
- Molecular Biological Research on the Pathogenic Mechanism of Retinoblastoma.Current issues in molecular biology · 2024Review
- miR-4529-3p Promotes the Progression of Retinoblastoma by Inhibiting RB1 Expression and Activating the ERK Signaling Pathway.Molecular biotechnology · 2024Article
- Long non-coding RNAs involved in retinoblastoma.Journal of cancer research and clinical oncology · 2023Review
- Article
- Long Non-coding RNA ZFPM2-AS1: A Novel Biomarker in the Pathogenesis of Human Cancers.Molecular biotechnology · 2022Review
- Oxidative Stress and Inflammation in Cardiovascular Diseases and Cancer: Role of Non-coding RNAs.The Yale journal of biology and medicine · 2022Review
- Role of non-coding RNAs and exosomal non-coding RNAs in retinoblastoma progression.Frontiers in cell and developmental biology · 2022Review
- lncRNA FOXD2-AS1 Promotes the Retinoblastoma Cell Viability and Migration by Sponging miR-31.BioMed research international · 2022Article
- HIV-infection and cocaine use regulate semen extracellular vesicles proteome and miRNAome in a manner that mediates strategic monocyte haptotaxis governed by miR-128 network.Cellular and molecular life sciences : CMLS · 2021Article
- Downregulation of MIAT reduces the proliferation and migratory and invasive abilities of retinoblastoma cells by sponging miR-665 and regulating LASP1.Experimental and therapeutic medicine · 2021Article
- Downregulation of Tim-1 inhibits the proliferation, migration and invasion of glioblastoma cells via the miR-133a/TGFBR1 axis and the restriction of Wnt/β-catenin pathway.Cancer cell international · 2021Article
- microRNA-362-3p targets USP22 to retard retinoblastoma growth via reducing deubiquitination of LSD1.Cell cycle (Georgetown, Tex.) · 2021Article
- 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
- Long Noncoding RNA ZFPM2-AS1 Knockdown Restrains the Development of Retinoblastoma by Modulating the MicroRNA-515/HOXA1/Wnt/β-Catenin Axis.Investigative ophthalmology & visual science · 2020Article
- Long Noncoding RNA HEIH Promotes Proliferation, Migration and Invasion of Retinoblastoma Cells Through miR-194-5p/WEE1 Axis.OncoTargets and therapy · 2020Article
- miR-214-3p Regulates Multi-Drug Resistance and Apoptosis in Retinoblastoma Cells by Targeting ABCB1 and XIAP.OncoTargets and therapy · 2020Article
Corrections and comments
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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
backgroundLong noncoding RNAs (lncRNAs) are dysregulated and play an important role in the tumorigenesis and progression of cancers. However, the potential roles of SNHG16 in retinoblastoma progression still remain largely unclear. MATERIALS AND
methodsThe expression levels of SNHG16, miR-182-5p, miR-128-3p and LASP1 in retinoblastoma tissues and cell lines were detected using qRT-PCR. The migratory and invasive abilities of retinoblastoma cells were assessed using Transwell assay. The regulatory relationships among SNHG16, miR-182-5p, miR-128-3p and LASP1 were analyzed through bioinformatics prediction and validated by luciferase reporter assay and Western blot.
resultsHere, we demonstrated that SNHG16 was frequently up-regulated in retinoblastoma tissue samples and cell lines. Clinicopathological features showed that high levels of SNHG16 were significantly associated with retinoblastoma metastasis and predicted poor overall survival. Functional studies demonstrated that knockdown of SNHG16 suppressed retinoblastoma cell migration and invasion. Mechanistic investigation revealed that SNHG16 exerted its oncogenic activity through increasing LASP1 expression and sponging miR-182-5p and miR-128-3p.
conclusionTaken together, our findings suggest SNHG16 as a novel biomarker and therapeutic target against retinoblastoma.
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