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MRNA expression signatures of human glioblastoma stem cell like cells after treatment with FG-3019, irradiation and FG-3019 + irradiation

ABSTRACT: To investigate effects on mRNA expression through treatment with FG-3019, irradiation and their combination to gain mechanistic hypotheses on the effects of these treatments on glioblastoma stem cell like cells which have been observed in vitro and in vivo. mRNA expression was measured 6 h after treatment with FG-3019, irradiation and their combination. 3 biological replicates were analyzed for each treatment condition (control, FG-3019, irratiation and FG-3019+irradiation)

ORGANISM(S): Homo sapiens

SUBMITTER: Roehrich Manuel

PROVIDER: S-ECPF-GEOD-60921 | biostudies-other |

REPOSITORIES: biostudies-other

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mRNA expression signatures of human glioblastoma stem cell like cells after treatment with FG-3019, irradiation and FG-3019 + irradiation

2014-08-30 | GSE60921 | GEO

mRNA expression signatures of human glioblastoma stem cell like cells after treatment with FG-3019, irradiation and FG-3019 + irradiation

Project description:To investigate effects on mRNA expression through treatment with FG-3019, irradiation and their combination to gain mechanistic hypotheses on the effects of these treatments on glioblastoma stem cell like cells which have been observed in vitro and in vivo. mRNA expression was measured 6 h after treatment with FG-3019, irradiation and their combination. 3 biological replicates were analyzed for each treatment condition (control, FG-3019, irratiation and FG-3019+irradiation)

2014-08-30 | E-GEOD-60921 | biostudies-arrayexpress

Cell Cycle Changes after Glioblastoma Stem Cell Irradiation: The Major Role of RAD51.

Project description:"Glioma Stem Cells" (GSCs) are known to play a role in glioblastoma (GBM) recurrence. Homologous recombination (HR) defects and cell cycle checkpoint abnormalities can contribute concurrently to the radioresistance of GSCs. DNA repair protein RAD51 homolog 1 (RAD51) is a crucial protein for HR and its inhibition has been shown to sensitize GSCs to irradiation. The aim of this study was to examine the consequences of ionizing radiation (IR) for cell cycle progression in GSCs. In addition, we intended to assess the potential effect of RAD51 inhibition on cell cycle progression. Five radiosensitive GSC lines and five GSC lines that were previously characterized as radioresistant were exposed to 4Gy IR, and cell cycle analysis was done by fluorescence-activated cell sorting (FACS) at 24, 48, 72, and 96 h with or without RAD51 inhibitor. Following 4Gy IR, all GSC lines presented a significant increase in G2 phase at 24 h, which was maintained over 72 h. In the presence of RAD51 inhibitor, radioresistant GSCs showed delayed G2 arrest post-irradiation for up to 48 h. This study demonstrates that all GSCs can promote G2 arrest in response to radiation-induced DNA damage. However, following RAD51 inhibition, the cell cycle checkpoint response differed. This study contributes to the characterization of the radioresistance mechanisms of GSCs, thereby supporting the rationale of targeting RAD51-dependent repair pathways in view of radiosensitizing GSCs.

| S-EPMC6213228 | biostudies-literature

The HIF1α/JMY pathway promotes glioblastoma stem-like cell invasiveness after irradiation.

Project description:Human glioblastoma (GBM) is the most common primary malignant brain tumor. A minor subpopulation of cancer cells, known as glioma stem-like cells (GSCs), are thought to play a major role in tumor relapse due to their stem cell-like properties, their high resistance to conventional treatments and their high invasion capacity. We show that ionizing radiation specifically enhances the motility and invasiveness of human GSCs through the stabilization and nuclear accumulation of the hypoxia-inducible factor 1α (HIF1α), which in turn transcriptionally activates the Junction-mediating and regulatory protein (JMY). Finally, JMY accumulates in the cytoplasm where it stimulates GSC migration via its actin nucleation-promoting activity. Targeting JMY could thus open the way to the development of new therapeutic strategies to improve the efficacy of radiotherapy and prevent glioma recurrence.

| S-EPMC7603339 | biostudies-literature

Expression profiling of glioblastoma cancer stem cells

Project description:Glioblastoma (GBM) is thought to be driven by a sub-population of cancer stem cells (CSCs) that self-renew and recapitulate tumor heterogeneity, yet remain poorly understood. Here we present a comparative epigenomic analysis of GBM CSCs that reveals widespread activation of genes normally held in check by Polycomb repressors. These activated targets include a large set of developmental transcription factors (TFs) whose coordinated activation is unique to the CSCs. We demonstrate that a critical factor in the set, ASCL1, activates Wnt signaling by repressing the negative regulator DKK1. We show that ASCL1 is essential for maintenance and in vivo tumorigenicity of GBM CSCs. Genomewide binding profiles for ASCL1 and the Wnt effector LEF1 provide mechanistic insight and suggest widespread interactions between the TF module and the signaling pathway. Our findings demonstrate regulatory connections between ASCL1, Wnt signaling and collaborating TFs that are essential for the maintenance and tumorigenicity of GBM CSCs. Two replicates for MGG4, MGG6, MGG23 and NS; four replicates for MGG8

| S-ECPF-GEOD-45899 | biostudies-other

Identification of Global DNA Methylation Signatures in Glioblastoma-Derived Cancer Stem Cells.

Project description:Glioblastoma (GBM) is the most common and most aggressive primary brain tumor in adults. The existence of a small population of stem-like tumor cells that efficiently propagate tumors and resist cytotoxic therapy is one proposed mechanism leading to the resilient behavior of tumor cells and poor prognosis. In this study, we performed an in-depth analysis of the DNA methylation landscape in GBM-derived cancer stem cells (GSCs). Parallel comparisons of primary tumors and GSC lines derived from these tumors with normal controls (a neural stem cell (NSC) line and normal brain tissue) identified groups of hyper- and hypomethylated genes that display a trend of either increasing or decreasing methylation levels in the order of controls, primary GBMs, and their counterpart GSC lines, respectively. Interestingly, concurrent promoter hypermethylation and gene body hypomethylation were observed in a subset of genes including MGMT, AJAP1 and PTPRN2. These unique DNA methylation signatures were also found in primary GBM-derived xenograft tumors indicating that they are not tissue culture-related epigenetic changes. Integration of GSC-specific epigenetic signatures with gene expression analysis further identified candidate tumor suppressor genes that are frequently down-regulated in GBMs such as SPINT2, NEFM and PENK. Forced re-expression of SPINT2 reduced glioma cell proliferative capacity, anchorage independent growth, cell motility, and tumor sphere formation in vitro. The results from this study demonstrate that GSCs possess unique epigenetic signatures that may play important roles in the pathogenesis of GBM.

| S-EPMC4648292 | biostudies-literature

PIM1 Inhibition Affects Glioblastoma Stem Cell Behavior and Kills Glioblastoma Stem-like Cells.

Project description:Despite comprehensive therapy and extensive research, glioblastoma (GBM) still represents the most aggressive brain tumor in adults. Glioma stem cells (GSCs) are thought to play a major role in tumor progression and resistance of GBM cells to radiochemotherapy. The PIM1 kinase has become a focus in cancer research. We have previously demonstrated that PIM1 is involved in survival of GBM cells and in GBM growth in a mouse model. However, little is known about the importance of PIM1 in cancer stem cells. Here, we report on the role of PIM1 in GBM stem cell behavior and killing. PIM1 inhibition negatively regulates the protein expression of the stem cell markers CD133 and Nestin in GBM cells (LN-18, U-87 MG). In contrast, CD44 and the astrocytic differentiation marker GFAP were up-regulated. Furthermore, PIM1 expression was increased in neurospheres as a model of GBM stem-like cells. Treatment of neurospheres with PIM1 inhibitors (TCS PIM1-1, Quercetagetin, and LY294002) diminished the cell viability associated with reduced DNA synthesis rate, increased caspase 3 activity, decreased PCNA protein expression, and reduced neurosphere formation. Our results indicate that PIM1 affects the glioblastoma stem cell behavior, and its inhibition kills glioblastoma stem-like cells, pointing to PIM1 targeting as a potential anti-glioblastoma therapy.

| S-EPMC8541331 | biostudies-literature

Expression data from glioblastoma stem cell clones (GSC)

Project description:Comparison of treatment sensitive GSC clones (TSGC) with treatment resistant GSC clones (TRGC). We used microarrays to identify molecular signatures of TRGC (upregulated genes). We used radiation treatment (RT) or RT plus TMZ to select treatment resistant GSC clones (TRGC)

| S-ECPF-GEOD-46531 | biostudies-other

Cell-type-specific signatures of microRNAs on target mRNA expression.

Project description:Although it is known that the human genome contains hundreds of microRNA (miRNA) genes and that each miRNA can regulate a large number of mRNA targets, the overall effect of miRNAs on mRNA tissue profiles has not been systematically elucidated. Here, we show that predicted human mRNA targets of several highly tissue-specific miRNAs are typically expressed in the same tissue as the miRNA but at significantly lower levels than in tissues where the miRNA is not present. Conversely, highly expressed genes are often enriched in mRNAs that do not have the recognition motifs for the miRNAs expressed in these tissues. Together, our data support the hypothesis that miRNA expression broadly contributes to tissue specificity of mRNA expression in many human tissues. Based on these insights, we apply a computational tool to directly correlate 3' UTR motifs with changes in mRNA levels upon miRNA overexpression or knockdown. We show that this tool can identify functionally important 3' UTR motifs without cross-species comparison.

| S-EPMC1413820 | biostudies-literature

Whole-genome mRNA expression profiling identifies functional and prognostic signatures in patients with mesenchymal glioblastoma multiforme.

Project description:BackgroundThe Cancer Genome Atlas (TCGA) has divided patients with glioblastoma multiforme (GBM) into four subtypes based on mRNA expression microarray. The mesenchymal subtype, with a larger proportion, is considered a more lethal one. Clinical outcome prediction is required to better guide more personalized treatment for these patients.AimsThe objective of this study was to identify a mRNA expression signature to improve outcome prediction for patients with mesenchymal GBM.ResultsFor signature identification and validation, we downloaded mRNA expression microarray data from TCGA as training set and data from Rembrandt and GSE16011 as validation set. Cox regression and risk-score analysis were used to develop the 4 signatures, which were function and prognosis associated as revealed by Gene Ontology (GO) analysis and Gene Set Variation Analysis (GSVA). Patients who had high-risk scores according to the signatures had poor overall survival compared with patients who had low-risk scores.ConclusionsThe signatures were identified as risk predictors that patients who had a high-risk score tended to have unfavorable outcome, demonstrating their potential for personalizing cancer management.

| S-EPMC6493663 | biostudies-literature

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