GEO DataSets

(Submitter supplied) Epidermal growth factor receptor (EGFR) signaling is constitutively activated in majority of GBM and is associated with a worse prognosis. Here we show that EGFR is responsible for overexpression of the m6A "reader" YTHDF2 in GBM through the EGFR/Src/ERK signaling pathway. YTHDF2 overexpression clinically correlates with poor glioma patient prognosis. EGFR signaling stabilizes YTHDF2 protein through phosphorylation of YTHDF2 serine 39 and threonine 381 by ERK1/2. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

4 Samples

Download data: XLSX

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL24676 GPL16791

8 Samples

Download data

(Submitter supplied) Epidermal growth factor receptor (EGFR) signaling is constitutively activated in majority of GBM and is associated with a worse prognosis. Here we show that EGFR is responsible for overexpression of the m6A "reader" YTHDF2 in GBM through the EGFR/Src/ERK signaling pathway. YTHDF2 overexpression clinically correlates with poor glioma patient prognosis. EGFR signaling stabilizes YTHDF2 protein through phosphorylation of YTHDF2 serine 39 and threonine 381 by ERK1/2. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

4 Samples

Download data: XLSX

(Submitter supplied) As a first step towards identifying the target genes of EGFR activity in glioma cells, genome-wide expression analyses were performed using the Affymetrix GeneChip Human Genome U133A array. To accomplish this, mRNA expression levels of these genes were measured in the glioblastoma cell lines, U87 and U178, engineered with EGFR by retrovirus transduction (termed U87-EGFR and U178-EGFR respectively), with or without 20 ng/mL EGF treatment for 3 h.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL96

8 Samples

Download data: CEL

(Submitter supplied) To gain insight into the molecular mechanisms underlying TRIP13-mediated oncogenic activity in GBM, we performed RNA-seq on spheres derived from U87MG-shTRIP13 and control cells .This analysis identified 1094 genes whose expression was markedly reduced by TRIP13 knockdown in U87MG-derived spheres (fold change >2, p < 0.05; Supplementary ). These downregulated genes were highly overrepresented in gene ontologies (GO) that are associated with growth factor activity, angiogenesis and chemotaxis. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20795

2 Samples

Download data: TXT

(Submitter supplied) This study uncovers a novel growth-promoting role of BCL6 in GBM, and provide the rationale of targeting BCL6 as a potential therapeutic approach for this deadly malignancy.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

4 Samples

Download data: TXT

(Submitter supplied) Epidermal Growth Factor Receptor (EGFR) gene amplification and mutations are the most common oncogenic events in Glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated epigenome and transcriptome analyses of cell lines, genotyped clinical samples and TCGA data, we show that EGFR mutations remodel the activated enhancer landscape of GBM, promoting tumorigenesis through a SOX9 and FOXG1-dependent transcriptional regulatory network in vitro and in vivo. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other

Platform:

GPL11154

87 Samples

Download data: BIGWIG, BW

(Submitter supplied) Although the oncogenic signalings driven by amplification and mutations of EGF receptor (EGFR) gene play a major role in glioblastoma pathogenesis, the responsible downstream mechanisms remain less clear. Here we demonstrate that tripartite motif-containing protein 59 (TRIM59), acting as a new downstream effector of EGFR signaling, regulates STAT3 activation in glioblastoma. EGFR signaling leads to TRIM59 upregulation through SOX9 that results in enhancing TRIM59 interaction with STAT3 in nucleus, and inhibiting STAT3 association with TC45 (the nuclear form of T cell protein tyrosine phosphatase TC-PTP), thereby maintaining STAT3 phosphorylation and activation and promoting tumorigenesis. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20795

4 Samples

Download data: XLSX

(Submitter supplied) As the crucial m6A reader, YTHDF2 usually degrades the target mRNAs by recognizing the m6A modified sites, consequently altering m6A levels of each mRNA. In this study, we used m6A MeRIP sequencing to detect the m6A modification alterations in prostate cancer (PCa) cell line after knocking down YTHDF2 and identify how YTHDF2 promote the PCa progression by mediating the mRNA degradation in m6A-dependent way.

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing; Other

Platform:

GPL20301

12 Samples

Download data: WIG

(Submitter supplied) Purpose: The splicing factor SRSF3 is a member of serine- and arginine-rich proteins, which is frequently upregulated in various types of cancer. The aim of this study is to profile the alternative splicing (AS) events that were regulated by SRSF3 in glioma stem-like cells (GSCs). Methods: Total RNAs isolated from GSC83 and GSC528 cells with SRSF3-konckout (KO) or control (WT) were subjected to paired-end RNA-seq using the Illumina NextSeq 500 system according to the manufacturer's instruction. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

4 Samples

Download data: TXT

(Submitter supplied) The diffuse invasion of glioblastoma (GBM) cells into healthy brain tissue is a main contributor for the high lethality of this most frequent form of malignant brain tumor. Plexins are cell surface receptors for semaphorins and control cell adhesion and cytoskeletal dynamics in development and in adult physiology. Gene expression of Plexin-B2 is upregulated in GBM and correlates with its lethality. We show here that Plexin-B2 activity can reduce the cohesiveness of GBM cells, which facilitates their invasive capacity. Targeted deletion of Plexin-B2 in GBM cells increased their cohesion to each other, revealing that a major function of Plexin-B2 activity is to downregulate cell-cell adhesion, possibly by downregulating other cell adhesion systems. In an in vivo intracranial transplant model, invasion of Plexin-B2 mutant GBM cells was impaired, with cells invading shorter distances. Interestingly, the loss of Plexin-B2 also changed the migration mode of cells, with the balance of cells in brain stroma vs. capillary space shifted: Plexin-B2 mutant cells were more likely to adhere to the vasculature. Our structure-function analyses revealed that the Ras-GAP domain of Plexin-B2 that is the main functional output responsible for the cohesion regulating function of Plexin-B2. Transcriptomic analyses of Plexin-B2 KO cells suggests that Plexin-B2 loss in different GBM cell lines has no direct transcriptional target genes, however, consistently, cell adhesion molecules were changed in expression, suggesting that cells compensate for loss of Plexin-B2. Thus, Plexin-B2 acts as a key regulator of the cohesiveness of GBM cells, thereby facilitating their invasiveness.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

29 Samples

Download data: TXT

(Submitter supplied) GBM cells derived from a patient were subjected to CLIP and RNAseq assays to for transcriptome analysis (CLIP and RNAseq).

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Other

Platforms:

GPL24676 GPL15520

36 Samples

Download data: BEDGRAPH

(Submitter supplied) N6-methyladenosine (m6A) is the most prevalent post-transcriptional modification on RNA. NK cells are the predominant innate lymphoid cells that mediate anti-viral and anti-tumor immunity. However, whether and how m6A modifications affect NK cell immunity remains unknown. Here, we discover that YTHDF2, a well-known m6A reader, is upregulated in NK cells upon activation by cytokines, tumors, and cytomegalovirus infection. more...

Organism:

Mus musculus

Type:

Other

Platform:

GPL17021

16 Samples

Download data: TXT

(Submitter supplied) Glioma cells and normal astrocytes were plated at low and high density to compare density-dependent gene expression.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL15207

28 Samples

Download data: CEL

(Submitter supplied) The analysis presented here aims at exposing single-cell transcriptome profiles of Drosophila larval brain type II neural stem cells (NSCII) and of their intermediate neural progenitor (INP) cell progeny during normal development and upon brain tumour initiation using the brain tumour (brat) mutant model. We have used brains 24 hours after larval hatching (ALH), a developmental stage when brat INPs (b_INP) have transformed into brain tumour initiating cells, expressing aberrantly the self-renewal transcription factor Deadpan unlike their iINP control counterparts (c_iINP), but have not yet started to overproliferate. more...

Organism:

Drosophila melanogaster

Type:

Expression profiling by array

Platform:

GPL14121

7 Samples

Download data: DAT

(Submitter supplied) The B cell to plasma cell transition relies on the coordinated remodelling of the gene expression program. We performed a CRISPR/Cas9 knockout screen of RNA binding proteins to identify post-transcriptional regulation of gene expression during the B cell terminal differentiation. The m6A binding protein YTHDF2 was identified as promoting B cell terminal differentiation. In the absence of YTHDF2 the germinal centre reaction is broadly intact, however, plasma cells fail to accumulate. more...

Organism:

Mus musculus

Type:

Methylation profiling by high throughput sequencing; Other

Platforms:

GPL17021 GPL24247

10 Samples

Download data: BED, TXT

(Submitter supplied) To elucidate molecular mechanisms that regulate the terminal differentiation of B cells into plasmablasts, we analysed how the B cell transcriptome changes during an in vitro culture system that mimics the germinal centre response (known as iGB culture). By culturing B cells on feeder cells expressing CD40L and B-cell activating factor BAFF in the presence of interleukin 4 and interleukin 21, this system allows class switch recombination to IgG1-producing cells and formation of CD138+ TACI+ B220low CD19int/low plasmablasts.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

6 Samples

Download data: TSV