Abstract
Despite of the discovery of protein therapeutic targets and advancement in multimodal therapy, the survival chance of high-risk neuroblastoma (NB) patients is still less than 50%. MYCN amplification is a potent driver of NB, which exerts its oncogenic activity through either activating or inhibiting the transcription of target genes. Recently, long noncoding RNAs (lncRNAs) are reported to be altered in cancers including NB. However, lncRNAs that are altered by MYCN amplification and associated with outcome in high-risk NB patients are limitedly discovered. Herein, we examined the expression profiles of lncRNAs and protein-coding genes between MYCN amplified and MYCN non-amplified NB from microarray (n = 47) and RNA-seq datasets (n = 493). We identified 6 lncRNAs in common that were differentially expressed (adjusted P ≤ 0.05 and fold change ≥ 2) and subsequently validated by RT-qPCR. The co-expression analysis reveals lncRNA, SNHG1 and coding gene, TAF1D highly co-expressed in NB. Kaplan-Meier analysis shows that higher expression of SNHG1 is significantly associated with poor patient survival. Importantly, multivariate analysis confirms high expression of SNHG1 as an independent prognostic marker for event-free survival (EFS) (HR = 1.58, P = 2.36E-02). In conclusion, our study unveils that SNHG1 is up-regulated by MYCN amplification and could be a potential prognostic biomarker for high-risk NB intervention.
Highlights
Neuroblastoma (NB) is a cancer of undifferentiated sympathetic neuroblasts that accounts for approximately 10% of all childhood cancer worldwide [1, 2]
LncRNAs that are altered by myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN) amplification and associated with outcome in high-risk NB patients are limitedly discovered
LncRNAs that are altered by MYCN amplification and associated with prognostication for high-risk NB are largely unknown
Summary
Neuroblastoma (NB) is a cancer of undifferentiated sympathetic neuroblasts that accounts for approximately 10% of all childhood cancer worldwide [1, 2]. The tumor either regress spontaneously in infants or undergo relentless proliferation in children older than 1 year of age, and is characterized by the patient’s age at diagnosis, spread of the disease or genetic heterogeneity led by chromosomal aberration, oncogene amplification or allelic loss [1,2,3] These diverse clinical presentations stratify NB tumors into risk groups in which low-risk group has a good prognosis and is cured by surgery alone, but high-risk group has a very poor prognosis despite of intensive chemotherapy [3,4,5]. There is a need to find new crucial players at the molecular level that can significantly associate with NB prognosis
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