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Transcriptomic analyis of SVG-p12 human fetal glial cells with overexpression of wildtype SOX10 or schwannoma-derived mutant isoforms

ABSTRACT: Transcriptomic analyis of SVG-p12 human fetal glial cells with overexpression of wildtype SOX10 or schwannoma-derived mutant isoforms

PROVIDER: PRJNA902337 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22311813_1.fastq.gz	Fastqsanger.gz
	SRR22311813_2.fastq.gz	Fastqsanger.gz
	SRR22311814_1.fastq.gz	Fastqsanger.gz
	SRR22311814_2.fastq.gz	Fastqsanger.gz
	SRR22311815_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analyis of SVG-p12 human fetal glial cells with overexpression of wildtype SOX10 or schwannoma-derived mutant isoforms

Project description:To investigate the gene expression changes caused by wildtype versus schwannoma-derived mutations in SOX10, we established SVG-p12 cell lines stably expressing either empty pCDF1 vector, wildtype SOX10, or two different mutant isoforms of SOX10. We then performed gene expression profiling analysis using RNA-seq for these SVG-p12 cell lines stably transduced with wildtype or mutant SOX10 isoforms.

2023-07-13 | GSE218097 | GEO

ChIP-seq analyis of SVG-p12 human fetal glial cells with exogenous expression of wildtype SOX10 or schwannoma-derived mutant isoforms

Project description:To investigate the chromatin binding patterns of wildtype SOX10 versus schwannoma-derived mutant isoforms, we established SVG-p12 cell lines stably expressing either FLAG epitope tagged wildtype SOX10 or two different mutant isoforms of SOX10. We then performed chromatin immunoprecipitation-DNA sequencing on these SVG-p12 cell lines stably transduced with wildtype or mutant SOX10 isoforms using an anti-FLAG epitope antibody.

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ChIP-seq analyis of SVG-p12 human fetal glial cells with exogenous expression of wildtype SOX10 or schwannoma-derived mutant isoforms

Project description:ChIP-seq analyis of SVG-p12 human fetal glial cells with exogenous expression of wildtype SOX10 or schwannoma-derived mutant isoforms

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Identification of Sox10 target genes by comparative expression profiling

Project description:RT4D6 Schwannoma cells were treated with siRNA specific for Sox10 and a mutant siRNA. Total RNA from the cells were used to screen for differentially expressed genes.

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Genomic Landscape of Schwannoma

Project description:Epigenome analysis of schwannoma tumor samples

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Transcription profiling of human SVG-A glial cells and SVGR2 glial cells

Project description:SVGR2 cells are glial cells which are derived from SVG-A cells. They were created by subjecting SVG-A cells to multiple rounds of lytic infection by the human polyomavirus JCV. SVGR2 cells are the cells that survived this process and are resistant to JCV infection. This experiment was designed to identify gene expression differences that may be responsible for SVGR2 resistance to JCV. Experiment Overall Design: SVG-A and SVGR2 cells are transformed cell lines. To eliminate gene expression differences that may have occurred due to genetic instability of these cell lines three subclones of each of the cell lines were created and used as a triplicate in the comparison. Total RNA was extracted from cells that had been left at 100% confluency for one day using the Qiagen RNeasy kit. cDNA was hybridized to the Affymetrix Human GeneChips U133A or U133B according to Affymetrix gudielines.

2008-11-07 | E-GEOD-7819 | biostudies-arrayexpress

Gene expression changes in HEI-193 (NF2-deficient Schwannoma) cells by Nf18001 or TEW7197 treatment.

Project description:Loss of NF2 (merlin) has been suggested as a genetic cause of neurofibromatosis type 2 and malignant peripheral nerve sheath tumor (MPNST). Previously, we demonstrated that NF2 sustained TGF- receptor 2 (TR2) expression and reduction or loss of NF2 activated non-canonical TGF- signaling, which reduced RKIP expression via TR1 kinase activity. Here, we show that a selective RKIP inducer (novel chemical, Nf18001) inhibits tumor growth and promotes schwannoma cell differentiation into mature Schwann cells under NF2-deficient conditions. In addition, Nf18001 is not cytotoxic to cells expressing NF2 and is not disturb canonical TGF- signaling. Moreover, the novel chemical induces expression of SOX10, a marker of differentiated Schwann cells, and promotes nuclear export and degradation of SOX2, a stem cell factor. Treatment with Nf18001 inhibited tumor growth in an allograft model with mouse schwannoma cells. These results strongly suggest that selective RKIP inducers could be useful for the treatment of neurofibromatosis type 2 as well as NF2-deficient MPNST. To know the global effect of Nf18001, we performed the microarray with HEI-193.

2021-10-22 | GSE186107 | GEO

Comparison of gene expression in SVG-A glial cells and SVGR2 glial cells

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Project description:JC virus (JCV) is a ubiquitous human polyomavirus that causes the demyelinating disease Progressive Multifocal Leukoencephalopathy (PML). JCV replicates in limited cell types in culture, predominantly in human glial cells. Thus, productive JCV infection is an indicator of the host cell transcription environment. Following introduction of a replication defective SV40 mutant that expressed large T protein into a heterogeneous culture of human fetal brain cells, multiple phenotypes became immortalized (SVG cells). A subset of SVG cells could support JCV replication. This mixed culture was called SVG cells. In the current study, clonal cell lines were selected from the original SVG cell culture. The SVG-5F4 clone showed low levels of viral growth. The SVG-10B1 clone was highly permissive for JCV DNA replication and gene expression. Microarray analysis revealed that viral infection did not significantly change gene expression in these cells. More resistant 5F4 cells expressed high levels of transcription factors known to inhibit JCV transcription. Interestingly, 5F4 cells highly expressed RNA of markers of Bergman or radial glia and 10B1 cells had high expression of markers of immature glial cells and activation of transcription regulators important for stem/progenitor cell self-renewal. These SVG-derived clonal cell lines provide a biologically relevant model to investigate cell type differences in JCV host range and pathogenesis, as well as neural development. 13 Human samples: 3 SVG 10B1 clones 14 days post mock-infection, 3 SVG 10B1 clones 14 days post JCV Mad-4 strain infection, 3 SVG 5F4 clones 14 days post mock-infection, 4 SVG 5F4 clones 14 days post JCV Mad-4 strain infection.

2013-10-17 | E-GEOD-45639 | biostudies-arrayexpress

Expression Patterns of SOX10 deficient BRAFi/MEKi tolerant and SOX10 KO A375 cell lines

Project description:Given the heterogeneous expression of SOX10 in naïve melanoma, we sought to characterize SOX10 deficient population. To this end, we generated SOX10 CRISPR/Cas9 knockouts using two different guide RNAs (gRNA, #2 and #4) in the A375 (BRAF mutant) metastatic cell line. Using this approach, we identified multiple clones with loss of SOX10 expression. RNA-seq was performed to characterize the SOX10-regulated transcriptome. We used GSEA analysis to evaluate significant pathway changes in SOX10 knockout cells when compared to parental cells. We observed an enrichment in pathways associated with the tumor microenvironment (epithelial-mesenchymal transition; TGF beta signaling; extracellular structure organization; apical junction; hypoxia; angiogenesis), alterations in metabolic pathways (increase in the glycolysis pathway), a reduction in MYC and E2F targets and upregulation in p53 pathway and TNFA signaling via NFkB in the SOX10 knockout cells compared to parental cells. SOX10 negative clones have been identified in the minimal residual disease in BRAF mutant PDX models following BRAF and MEK inhibition and in patient samples while on treatment and SOX10 loss has been described as a resistant mechanism in BRAF mutant melanoma patients following vemurafenib treatment. Thus, we also analyzed the transcriptome profile of SOX10 low/deficient cells that arose following BRAFi+MEKi treatment in vivo. We performed GSEA analysis on RNA-seq data of CRT34 and CRT35 cells compared to parental A375 cells. CRT34 and CRT35 showed a very similar transcriptome profile to SOX10 KO cells when compared to A375 parental cells

2022-01-24 | GSE180568 | GEO

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