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Sense-antisense lncRNA pair encoded by locus 6p22.3 determines neuroblastoma susceptibility via the USP36-CHD7-SOX9 regulatory axis

Journal article
Authors Tanmoy Mondal
Prasanna Kumar Juvvuna
Agnete Kirkeby
Sanhita Mitra
Subazini Thankaswamy Kosalai
Larissa Traxler
Falk Hertwig
Sara Wernig-Zorc
Caroline Miranda
Lily Deland
Christoph Bartenhagen
Ruth Volland
Deniz Bartsch
Sashidar Bandaru
Anne Engesser
Santhilal Subhash
Tommy Martinsson
Helena Carén
Levent Akyürek
Leo Kurian
Meena Kanduri
Maite Huarte
Per Kogner
Matthias Fischer
Chandrasekhar Kanduri
Published in Cancer Cell
Volume 33
Issue 3
Pages 417-434.e7
ISSN 1535-6108
Publication year 2018
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Biomedicine, Department of Pathology
Sahlgrenska Cancer Center
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 417-434.e7
Language en
Keywords lncRNA, neuroblastoma, long noncoding RNA, Cancer, epigenetics,
Subject categories Medical Genetics, Health Sciences, Clinical Medicine, Medicinal Chemistry, Medical Biotechnology, Cell and Molecular Biology, Neurosciences


Trait-associated loci often map to genomic regions encoding long noncoding RNAs (lncRNAs), but the role of these lncRNAs in disease etiology is largely unexplored. We show that a pair of sense/antisense lncRNA (6p22lncRNAs) encoded by CASC15 and NBAT1 located at the neuroblastoma (NB) risk-associated 6p22.3 locus are tumor suppressors and show reduced expression in high-risk NBs. Loss of functional synergy between 6p22lncRNAs results in an undifferentiated state that is maintained by a gene-regulatory network, including SOX9 located on 17q, a region frequently gained in NB. 6p22lncRNAs regulate SOX9 expression by controlling CHD7 stability via modulating the cellular localization of USP36, encoded by another 17q gene. This regulatory nexus between 6p22.3 and 17q regions may lead to potential NB treatment strategies.

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