The Risk-Associated Long Noncoding RNA NBAT-1 Controls Neuroblastoma Progression by Regulating Cell Proliferation and Neuronal Differentiation.
Journal article, 2014

Neuroblastoma is an embryonal tumor of the sympathetic nervous system and the most common extracranial tumor of childhood. By sequencing transcriptomes 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.

NBAT-1

NBAT1

Epigenetics

Neuroblastoma

NBAT

long noncoding RNA

Author

Gaurav Kumar Pandey

University of Gothenburg

Sanhita Mitra

University of Gothenburg

Santhilal Subhash

University of Gothenburg

Falk Hertwig

Meena Kanduri

University of Gothenburg

Kankadeb Mishra

University of Gothenburg

Susanne Fransson

University of Gothenburg

Abiarchana Ganeshram

University of Gothenburg

Tanmoy Mondal

University of Gothenburg

Sashidar Bandaru

University of Gothenburg

Malin Östensson

University of Gothenburg

Levent Akyürek

University of Gothenburg

Jonas Abrahamsson

Susan Pfeifer

E. G. Larsson

University of Gothenburg

Leming Shi

Zhiyu Peng

Matthias Fischer

Tommy Martinsson

University of Gothenburg

Fredrik Hedborg

Per Kogner

Chandrasekhar Kanduri

University of Gothenburg

Cancer Cell

1535-6108 (ISSN)

Vol. 26 5 722-737

Subject Categories

Biochemistry and Molecular Biology

DOI

10.1016/j.ccell.2014.09.014

PubMed

25517750

More information

Created

10/10/2017