GEO DataSets

(Submitter supplied) The main scientific objective of the project was to investigate whether Lamin A/C could be involved in neuroblastoma differentiation. Moreover, taking into account the significance of differentiation stage in the neuroblastoma tumor progression we have also studied a possible role of Lamin A/C in the tumorigenesis of this neuronal cancer. As differentiating stimulus we used the all-trans retinoic acid (RA), the most effective compound which has been shown to induce differentiation in neuroblastoma cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6480

6 Samples

Download data: TXT

(Submitter supplied) The mouse neuroblastoma N18TG2 clone is unable to differentiate and defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

8 Samples

Download data: TXT

(Submitter supplied) In adult cancers, epigenetic changes and aberrant splicing of the DNMT3B is commonly observed, and the pattern of gene methylation and expression has been shown to be modified by DNMT3B7, a truncated protein of DNMT3B. Much less is known about the mechanism of epigenetic changes in the pediatric cancer neuroblastoma. To investigate if aberrant DNMT3B transcripts alter DNA methylation, gene expression and tumor phenotype in neuroblastoma, we measured DNMT3B isoform expression in primary tumors and cell lines. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL9115

3 Samples

Download data: TAR

(Submitter supplied) Analyses of the effect of CRISPR/CAS9 mediated knock out of the EMT-transcription factor SNAI2 on the mRNA expression profile of human neuroblastoma SH-SY5Y cells to identify genes that are differentially expressed upon loss of SNAI2. Results provide insight into genes that are repressed by SNAI2 in neuroblastoma cells under normal culture conditions, where loss of SNAI2 enhances the expression of genes involved in biological processes such as neuron development and neuron differentiation.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

9 Samples

Download data: TXT

(Submitter supplied) Single-color gene expression profiles from IMR-32 neuroblastoma cell lines were generated using 44K oligonucleotide microarrays. To gain insights into the molecular processes occurring upon TFAP2B re-expression, we performed gene expression measurements in TFAP2B and GFP expressing transgenic IMR-32 neuroblastoma cell lines at d2 and d7 of transgene induction.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL16876

4 Samples

Download data: TXT

(Submitter supplied) The polycomb repressor complex 2 molecule EZH2 is now known to play a role in essential cellular processes, namely, cell fate decisions, cell cycle regulation, senescence, cell differentiation, and cancer development/progression. EZH2 inhibitors have recently been developed; however, their effectiveness and underlying molecular mechanisms in many malignancies have not yet been elucidated in detail. Although the functional role of EZH2 in tumorigenesis in neuroblastoma (NB) has been investigated, mutations of EZH2 have not been reported. A Kaplan-Meier analysis on the event free- and overall survival of NB patients indicated that the highexpression of EZH2 correlated with an unfavorable prognosis. In order to elucidate the functional roles of EZH2 in NB tumorigenesis and its aggressiveness, we knocked down EZH2 in NB cell lines using lentivirus systems. The knockdown of EZH2 significantly induced NB cell differentiation, e.g. neurite extension, and the neuronal differentiation markers, NF68 and GAP43. EZH2 inhibitors also induced NB cell differentiation. We performed a comprehensive transcriptome analysis using Human Gene Expression Microarrays and found that NTRK1 (TrkA) is one of the EZH2-related suppression targets. The depletion of NTRK1 canceled EZH2 knockdown-induced NB cell differentiation. Our integrative methylome, transcriptome, and chromatin immunoprecipitation assays using NB cell lines and clinical samples clarified that the NTRK1 P1 and P2 promoter regions were regulated differently by DNA methylation and EZH2-related histone modifications. The NTRK1 transcript variants 1/2, which were regulated by EZH2-related H3K27me3 modifications at the P1 promoter region, were strongly expressed in favorable, but not unfavorable NB. The depletion and inhibition of EZH2 successfully induced NTRK1 transcripts and functional proteins. Collectively, these results indicate that EZH2 plays important roles in preventing the differentiation of NB cells and also that EZH2-related NTRK1 transcriptional regulation may be the key pathway for NB cell differentiation.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL16699

18 Samples

Download data: TXT

(Submitter supplied) Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through mining public microarray and RNA sequencing datasets, we identified neuroblastoma highly expressed 1 (NHEG1) as a novel 1360-bp lncRNA associated with poor outcome of NB. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17586

6 Samples

Download data: CEL

(Submitter supplied) Derangement of cellular differentiation due to mutation or inappropriate expression of specific genes is a common feature in tumours. Here, we show that depletion of ZNF281 induces neuronal differentiation of neuroblastoma cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL21185

8 Samples

Download data: TXT

(Submitter supplied) A neuroblasoma cell line, NB-1, was treated with a DNA demethylating agents (5-aza-2'-deoxycytidine: 5-aza-dC). Genome-wide DNA methylation was analyzed using the Infinium HumanMethylation450 BeadChip.

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL13534

2 Samples

Download data: IDAT

(Submitter supplied) A neuroblasoma cell line, TGW, was treated with a DNA demethylating agents (5-aza-2'-deoxycytidine: 5-aza-dC). Genome-wide DNA methylation was analyzed using the Infinium Human MethylationEPIC BeadChip.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL21145

2 Samples

Download data: IDAT

(Submitter supplied) A neuroblastoma cell line, NB-1, was treated with mock, a DNA demethylating agent (5-aza-2'-deoxycytidine: 5-aza-dC), a synthetic retinoic acid (tamibarotene: TBT), and the combination of 5-aza-dC and TBT. A genome-wide gene expression analysis was performed using SurePrint G3 Human Gene Expression 8 x 60K v2 Microarray.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17077

4 Samples

Download data: TXT

(Submitter supplied) Neuroblastoma (NB) arises from neural crest cells (NCCs) secondary to a block in differentiation. Retinoic acid (RA) differentiation therapy has limited therapeutic efficacy, and the mechanisms preventing terminal differentiation remain elusive. We found that the chromatin modifier CHAF1A restricts neuronal differentiation and promotes NB oncogenesis. CHAF1A blocks NC differentiation into mature neurons in both human NCCs and zebrafish models. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL16686

12 Samples

Download data: CEL