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dc.contributor.authorBhavsar, Swapnil Parashram
dc.contributor.authorLøkke, Cecilie
dc.contributor.authorFlægstad, Trond
dc.contributor.authorEinvik, Christer
dc.date.accessioned2019-02-05T12:58:30Z
dc.date.available2019-02-05T12:58:30Z
dc.date.issued2018-09-11
dc.description.abstractHigh‑risk neuroblastoma is the most aggressive form of cancer in children. The estimated survival of children with high‑risk neuroblastoma is 40‑50% compared with low and intermediate risk neuroblastoma, which is >98 and 90‑95%, respectively. In addition, patients with high‑risk neuroblastoma often experience relapse following intensive treatments with standard chemotherapeutic drugs. Therefore alternative strategies are required to address this problem. MicroRNAs (miRNAs/miRs) are small, endogenously expressed non‑coding RNAs, which when deregulated have been demonstrated to serve significant roles in the tumorigenesis of a number of different types of cancer. Results from a previous deep sequencing study identified 22 downregulated miRNAs from the 14q32 miRNA cluster differentially expressed in neuroblastoma cell lines isolated from 6 patients at diagnosis and at relapse following intensive treatments. miR‑376c‑3p is one of the 22 miRNAs that was downregulated in the majority of the cell lines isolated from patients post treatment. The present study employed reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) to quantify the basic expression of miR‑376c‑3p in 6 neuroblastoma cell lines. The functional role of miR‑376c‑3p in the neuroblastoma cell lines was evaluated by alamar blue‑cell viability and propidium iodide‑flow cytometric assays. In addition, luciferase reporter assays, RT‑qPCR and western blotting were performed to identify and quantify the targets of miR‑376c‑3p in neuroblastoma cell lines. Ectopic expression of miR‑376c‑3p led to significant inhibition of cell viability and G1‑cell cycle arrest in multiple neuroblastoma cell lines by reducing the expression of cyclin D1, an oncogene critical for neuroblastoma pathogenesis. The results of the present study provide novel insights into the functional role of miR‑376c‑3p and suggest new approaches for the treatment of neuroblastoma.en_US
dc.description.sponsorshipNorthern-Norway Health Authoritiesen_US
dc.descriptionThe following article, Bhavsar, S.P., Løkke, C., Flægstad, T. & Einvik, C. (2018). Hsa-miR-376c-3p targets cyclin D1 and induces G1-cell cycle arrest in neuroblastoma cells. <i>Oncology Letters, 16</i>(5), 6786-6794, can be accessed at <a href=https://doi.org/10.3892/ol.2018.9431> https://doi.org/10.3892/ol.2018.9431</a>.en_US
dc.identifier.citationBhavsar, S.P., Løkke, C., Flægstad, T. & Einvik, C. (2018). Hsa-miR-376c-3p targets cyclin D1 and induces G1-cell cycle arrest in neuroblastoma cells. <i>Oncology Letters, 16</i>(5), 6786-6794. https://doi.org/10.3892/ol.2018.9431en_US
dc.identifier.cristinIDFRIDAID 1630631
dc.identifier.doi10.3892/ol.2018.9431
dc.identifier.issn1792-1074
dc.identifier.issn1792-1082
dc.identifier.urihttps://hdl.handle.net/10037/14622
dc.language.isoengen_US
dc.publisherSpandidos Publicationsen_US
dc.relation.journalOncology Letters
dc.rights.accessRightsopenAccessen_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Oncology: 762en_US
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Onkologi: 762en_US
dc.subjecthigh-risk neuroblastomaen_US
dc.subjectmicroRNAen_US
dc.subjectdeep sequencingen_US
dc.subject14q32 microRNA clusteren_US
dc.subjectmicroRNA-376c-3pen_US
dc.subjectCyclin D1en_US
dc.titleHsa-miR-376c-3p targets cyclin D1 and induces G1-cell cycle arrest in neuroblastoma cellsen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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