ArticleOncoTargets and therapy2020
MicroRNA-16 Inhibits Glioblastoma Growth in Orthotopic Model by Targeting Cyclin D1 and WIP1.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- In Silico Identification of circPIM1/miR-16-5p/miR-195-5p/PIM1 Feed-Forward Loop in Recurrent Grade 2 Meningioma.International journal of molecular sciences · 2025Article
- Saturation transfer (CEST and MT) MRI for characterization of U-87 MG glioma in the rat.NMR in biomedicine · 2025Article
- MicroRNAs miR-16 and miR-519 control meningioma cell proliferationFrontiers in oncology · 2023Article
- Identification of a novel circular RNA circZNF652/miR-486-5p/SERPINE1 signaling cascade that regulates cancer aggressiveness in glioblastoma (GBM).Bioengineered · 2022Article
- Highly Invasive Fluorescent/Bioluminescent Patient-Derived Orthotopic Model of Glioblastoma in Mice.Frontiers in oncology · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTo examine the molecular mechanism by which miRNA-16 (miR-16) suppresses glioblastoma in vitro and in vivo.
methodsGene expression of miR-16 in normal brain tissues and human glioma cell lines was examined. To characterize the functional role of miR-16 in vitro, miR-16 was ectopically expressed in U87 cells by lentiviral transduction. Expression of miR-16 downstream targets cyclin D1 and Bcl-2 in U87 was studied using Western blotting. Cell proliferation and clonogenic property were examined using CCK-8 and clone formation assay, respectively. Migration and invasiveness of U87 was studied using wound-healing assay and transwell assay, respectively. In vivo tumorigenic properties of the miR-16-transduced U87 cells were examined in an orthotopic xenograft model. Immunohistochemistry was performed to examine cyclin D1, WIP1 and CD31 expressions.
resultsExpression of miR-16 was reduced in glioblastoma cell lines compared to normal human brain tissues. Ectopic miR-16 expression reduced cyclin D1 and Bcl-2 in U87 cells. miR-16 also induced apoptosis, reduced cell proliferation and clone formation. Furthermore, miR-16 suppressed U87 migration in wound-healing assay and invasion across transwell membrane in vitro. In an orthotopic tumor model, overexpression of miR-16 inhibited tumor growth in vivo was accompanied with reduction in cyclin D1 and WIP1 expression in the xenografts. CD31 expression in miR-16-overexpressed xenografts was also decreased. The determined microvessel density of the miR-16 overexpression group was significantly lower than those groups treated with vehicle and empty vector. DISCUSSION: MicroRNA-16 exhibits inhibitory effects of glioblastoma. MicroRNA-16 and its downstream targets could be potential therapeutic targets for treatment of glioblastoma.
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