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The Risk-Associated Long Noncoding RNA NBAT-1Controls Neuroblastoma Progression by RegulatingCell Proliferation and Neuronal Differentiation
Department of Medical Genetics, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Sweden.
Department of Medical Genetics, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Sweden.
Department of Medical Genetics, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Sweden.
Department of Pediatric Hematology and Oncology, University Children’s Hospital of Cologne, and Center for Molecular Medicine Cologne, University of Cologne, Germany.
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2014 (English)In: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 26, no 5, 722-737 p.Article in journal (Refereed) Published
Abstract [en]

Neuroblastoma is an embryonal tumor of the sympathetic nervous system and the most common extracranial tumor of childhood. By sequencing transcriptonnes of low- and high-risk neuroblastomas, we detected differentially expressed annotated and nonannotated long noncoding RNAs (lncRNAs). We identified a lncRNA neuroblastoma associated transcript-1 (NBAT-1) as a biomarker significantly predicting clinical outcome of neuroblastoma. CpG methylation and a high-risk neuroblastoma associated SNP on chromosome 6p22 functionally contribute to NBAT-1 differential expression. Loss of NBAT-1 increases cellular proliferation and invasion. It controls these processes via epigenetic silencing of target genes. NBAT-1 loss affects neuronal differentiation through activation of the neuronal-specific transcription factor NRSF/REST. Thus, loss of NBAT-1 contributes to aggressive neuroblastoma by increasing proliferation and impairing differentiation of neuronal precursors.

Place, publisher, year, edition, pages
2014. Vol. 26, no 5, 722-737 p.
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Cancer and Oncology
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URN: urn:nbn:se:uu:diva-238013DOI: 10.1016/j.ccell.2014.09.014ISI: 000344980900015PubMedID: 25517750OAI: oai:DiVA.org:uu-238013DiVA: diva2:769825
Available from: 2014-12-09 Created: 2014-12-09 Last updated: 2017-12-05Bibliographically approved

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Pfeifer, SusanHedborg, Fredrik

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