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Links from GEO DataSets

Items: 10

1.

RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells

(Submitter supplied) We performed RNA-seq to determine the impact of MOB2 depletion on global gene expression profile.The results reveal that dysregulated genes were enriched for genes related to pathways in cancer, including PI3K–AKT signaling, cell adhesion molecules (CAMs), focal adhesion and cytokine-cytokine interaction.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: TXT
2.

RNA sequencing analysis of SF-539-shControl and SF-539-shFKBP9 cells

(Submitter supplied) We performed RNA-seq to determine the impact of FKBP9 depletion on global gene expression profile. The results show knock down of FKBP9 activated ER stress or UPR signaling related genes.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
2 Samples
Download data: TXT
3.

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and TWIST1 knock out U87 xenograft mice transcriptomes

(Submitter supplied) Purpose:Next-generation sequencing has revolutionized sytems-level celluar pathway analysis. The goals of this study are to compare the U87 cell xenograft GBM mice (U87 cell line) to TWIST1 knock out U87 cell xenograft GBM mice (TWIST1 knock out U87 cell line) using their transcriptomes
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
23 Samples
Download data: TXT
4.

Expression data of J3T-1, J3T-2, J3T-1shA, J3T-2A glioma

(Submitter supplied) We have previously established two sibling glioma subclones, J3T-1 and J3T-2, showing distinct invasive and angiogenic phenotypes. J3T-1, expressing high annexin A2, demonstrates robust angiogenesis and tumor invasion around neovasculature. J3T-2, expressing low annexin A2, demonstrates diffuse invasion along white matter tracts. Knockdown of annexin A2 in J3T-1 (J3T-1shA) resulted in diffuse invasion pattern, and overexpression of annexin A2 in J3T-2 (J3T-2A) showed prominent angiogenesis. more...
Organism:
Canis lupus familiaris
Type:
Expression profiling by array
Platform:
GPL3738
4 Samples
Download data: CEL
Series
Accession:
GSE138374
ID:
200138374
5.

Expression data for miR-33a over-expression in CD133-negative D456MG cells

(Submitter supplied) MiR-33a is involved in the maintenance of Glioma Initiating Cells (GIC) and tumor progression. MicroRNA-33a could promote GIC growth and self-renewal by regulating two pathways including cAMP/PKA pathway and Notch pathway. We used microarrays to identify the direct target genes of miR-33a in a glioblastoma cell line D456MG. We used microarrays to detail the global change of gene expression after miR-33a over-expression and identified target genes during this process.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
2 Samples
Download data: CEL
Series
Accession:
GSE59484
ID:
200059484
6.

Annexin 2A sustains glioblastoma cell dissemination and proliferation affecting patient prognosis

(Submitter supplied) Glioblastoma (GBM) is the most devastating tumour of the brain, endowed with a fatal prognosis. Indeed, the complete eradication of cancer cell disseminated outside the GBM mass still remains a crucial issue. Given the reported strong association existing between Annexin 2A (ANXA2) expression and cell dissemination in many cancers, we evaluated the effects exerted by the modulation of ANXA2 levels in GBM cells and assessed its potential in predicting patient outcome. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
8 Samples
Download data: CEL
Series
Accession:
GSE76786
ID:
200076786
7.

Anti-Warburg effect elicited by mitochondrial biogenesis drives differentiation of glioblastoma cells into astroglial cells

(Submitter supplied) Glioblastoma (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed to be potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established the induced differentiation model of GBM by using cAMP activators, which specifically directed GBM into astroglia. Next, transcriptomic and proteomic analyses uncovered oxidative phosphorylation and mitochondrial biogenesis were involved in induced differentiation of GBM. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
5 Samples
Download data: TXT
8.

Plexin-B2 reduces glioma cell cohesion and regulates glioma-vascular interactions

(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
9.

Expression data from orthotopic U-87 MG xenograft mouse models

(Submitter supplied) Glioblastoma (GBM) is classified as World Health Organization grade IV tumors of the central nervous system, and it is the most malignant form of glioma. The current GBM therapies could not completely eliminate the tumor mass and the occurrence of therapeutic resistance of surviving GBM cells is considered as an obstacle to be overcome. We used microarrays to detail the global program of gene expression underlying development of radioresistance of GBM and identified a variety of genes whose expressions were regulated during this process.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
2 Samples
Download data: CEL
Series
Accession:
GSE117126
ID:
200117126
10.

Targeting the Sphingolipid Balance via Acid Ceramidase Inhibition toDecrease Growth of TMZ-Resistant Glioblastoma and Block Migration

(Submitter supplied) We performed 3'RNAseq on U251T or U251P cells treated with vehicle or carmofur.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: CSV
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