Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ZNF281 inhibits neuronal differentiation

ABSTRACT: 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(S): Homo sapiens

PROVIDER: GSE112029 | GEO | 2018/06/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

ZNF281 inhibits neuronal differentiation

Project description:ZNF281 inhibits neuronal differentiation

| PRJNA438998 | ENA

Neuroblastoma-associated mutations in Drosophila Alk peturb neuronal differentiation and promote neuronal survival.

Project description:Neuroblastoma-associated mutations in Drosophila Alk peturb neuronal differentiation and promote neuronal survival.

| PRJNA817171 | ENA

Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression [array]

Project description:Neuroblastoma is a pediatric cancer characterized by variable outcomes ranging from spontaneous regression to life-threatening progression. High-risk neuroblastoma patients receive myeloablative chemotherapy with hematopoietic stem-cell transplant followed by adjuvant retinoid differentiation treatment. However, the overall survival remains low; hence, there is an urgent need for alternative therapeutic approaches. One feature of high-risk neuroblastoma is the high level of DNA methylation of putative tumor suppressors. Combining the reversibility of DNA methylation with the differentiation-promoting activity of retinoic acid (RA) could provide an alternative strategy to treat high-risk neuroblastoma. Here we show that treatment with the DNAdemethylating drug 5-Aza-deoxycytidine (AZA) restores high-risk neuroblastoma sensitivity to RA. Combined systemic distribution of AZA and RA impedes tumor growth and prolongs survival. Genomewide analysis of treated tumors reveals that this combined treatment rapidly induces a HIF2α-associated hypoxia-like transcriptional response followed by an increase in neuronal gene expression and a decrease in cell-cycle gene expression. A small-molecule inhibitor of HIF2α activity diminishes the tumor response to AZA+RA treatment, indicating that the increase in HIF2α levels is a key component in tumor response to AZA+RA. The link between increased HIF2α levels and inhibited tumor growth is reflected in large neuroblastoma patient datasets. Therein, high levels of HIF2α, but not HIF1α, significantly correlate with expression of neuronal differentiation genes and better prognosis but negatively correlate with key features of high-risk tumors, such as MYCN amplification. Thus, contrary to previous studies, our findings indicate an unanticipated tumor-suppressive role for HIF2α in neuroblastoma.

2017-08-23 | GSE102994 | GEO

Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression [RNA-Seq]

Project description:Neuroblastoma is a pediatric cancer characterized by variable outcomes ranging from spontaneous regression to life-threatening progression. High-risk neuroblastoma patients receive myeloablative chemotherapy with hematopoietic stem-cell transplant followed by adjuvant retinoid differentiation treatment. However, the overall survival remains low; hence, there is an urgent need for alternative therapeutic approaches. One feature of high-risk neuroblastoma is the high level of DNA methylation of putative tumor suppressors. Combining the reversibility of DNA methylation with the differentiation-promoting activity of retinoic acid (RA) could provide an alternative strategy to treat high-risk neuroblastoma. Here we show that treatment with the DNA demethylating drug 5-Aza-deoxycytidine (AZA) restores high-risk neuroblastoma sensitivity to RA. Combined systemic distribution of AZA and RA impedes tumor growth and prolongs survival. Genomewide analysis of treated tumors reveals that this combined treatment rapidly induces a HIF2α-associated hypoxia-like transcriptional response followed by an increase in neuronal gene expression and a decrease in cell-cycle gene expression. A small-molecule inhibitor of HIF2α activity diminishes the tumor response to AZA+RA treatment, indicating that the increase in HIF2α levels is a key component in tumor response to AZA+RA. The link between increased HIF2α levels and inhibited tumor growth is reflected in large neuroblastoma patient datasets. Therein, high levels of HIF2α, but not HIF1α, significantly correlate with expression of neuronal differentiation genes and better prognosis but negatively correlate with key features of high-risk tumors, such as MYCN amplification. Thus, contrary to previous studies, our findings indicate an unanticipated tumor-suppressive role for HIF2α in neuroblastoma.

2017-06-28 | GSE100568 | GEO

Human BE(2)-C neuronal responses to type I IFN stimulation

Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to retinoic acid-induced differentiation and type I IFN stimulation.

2009-07-01 | GSE16450 | GEO

Neuronal differentiation of DFATs

Project description:Neuronal differentiation of DFATs

| PRJNA417063 | ENA

Human BE(2)-C neuronal responses to WEEV infection

Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to infection with western equine encephalitis virus (WEEV).

2009-07-01 | GSE16451 | GEO

Quantitative proteomic analysis identifies proteins and pathways related to neuronal development in differentiated SH-SY5Y neuroblastoma cells

Project description:SH-SY5Y neuroblastoma cells are widely used as in vitro neuronal model. They can be induced to a differentiated phenotype, presenting neurites and synaptical-like structures in response to retinoic (RA) acid and brain-derived neurotrophic factor (BDNF), providing a model to analyze neuronal differentiation. We report a large scale MS quantification of SH-SY5Y cells proteome during its differentiation process after treatment with RA/BDNF. Using isobaric tags for relative and absolute quantification (iTRAQ) approach and phosphopeptide enrichment protocols, we identified a total of 5587 proteins, 366 of them showed differential abundance between both conditions of culture. Differentiated SH-SY5Y cells showed regulation of proteins and phosphosites strongly related to neuronal development, in contrast, undifferentiated cells expressed proteins more related to cell proliferation and control of cell cycle. Interactive network analysis covered processes as focal adhesion, cytoskeleton dynamics and neurodegenerative diseases and pathway analysis displayed regulation of mitogen-activated protein kinase and phosphoinositide 3-kinase/Akt signaling pathways mainly; the proteins involved in those processes might be considered as markers for neuronal differentiation. Overall the data collection presented here can be explored for any studies which intent to use SH-SY5Y as neuronal model.

| MSV000080133 | MassIVE

CHAF1A Blocks Neuronal Differentiation and Promotes Neuroblastoma Oncogenesis via Metabolic Reprogramming

Project description:CHAF1A Blocks Neuronal Differentiation and Promotes Neuroblastoma Oncogenesis via Metabolic Reprogramming

| PRJNA603348 | ENA

HOXC9-induced neuronal differentiation in human neuroblastoma BE(2)-C cells

Project description:HOXC9-induced neuronal differentiation in human neuroblastoma BE(2)-C cells

| PRJNA149551 | ENA