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IL-6 derived from therapy-induced senescence facilitates the glycolytic phenotype in glioblastoma cells

ABSTRACT: In this study, we aimed to determine the fate of GBM cells following cAMP-induced differentiation. We assessed the effect of dbcAMP treatment on the global gene expression pattern of the human GBM cell lines DBTRG and U87 using RNA sequencing (RNA-Seq) analysis

ORGANISM(S): Homo sapiens

PROVIDER: GSE146197 | GEO | 2020/03/03

REPOSITORIES: GEO

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Gene expression of DBTRG-05MG treated with dbcAMP or miR-1275 mimics

Project description:Samples 1-5 were the microRNA-seq data of DBTRG-05MG treated with dbcAMP at 0/6/12/24/48 hours. Sample 6-17 were the analysis of DBTRG-05MG cells treated with control-media, dbcAMP, miR-1275 mimics and combined dbcAMP and miR-1275 mimics on day3.

2018-08-29 | GSE119161 | GEO

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

Project description: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. Further investigation showed dbcAMP reversed Warburg effect evidenced by increase of oxygen consumption and reduction of lactate production. Stimulated mitochondrial biogenesis downstream of CREB/PGC1α pathway triggered metabolic shift and differentiation. Blocking mitochondrial biogenesis by mdivi1 or silencing PGC1α abrogated differentiation, reversely over-expression of PGC1α elicited differentiation. In GBM xenograft models and patient-derived GBM samples, cAMP activators also induced tumor growth inhibition and differentiation. This study shows mitochondrial biogenesis and metabolic switch to oxidative phosphorylation drive the differentiation process of tumor cells.

2017-11-10 | GSE89745 | GEO

Gene profile of glioblastoma cells treated with y15 and temozolomide

Project description:The gene expression profiles were identified in glioblastoma cells treated with FAK inhibitor Y15, temozolomide alone or with combination of Y15 and Temozolomide DBTRG and U87 were treated with FAK inhibitor Y15 at 10 microM for 24 h; U87 cells were treated with Temozolomide 100 microM for 24 h and Y15+temozolomide at the same dose as each agent alone

2013-01-12 | E-GEOD-43452 | biostudies-arrayexpress

Human Mesenchymal Stem Cells Exploit the Immune Response Mediating Chemokines to Impact the Phenotype of Glioblastoma

Project description:Four human mesenchymal stem cells (hMSC) clones (MSC-1, MSC-2, MSC-3, MSC-4) and three different glioblastoma multiformae (GBM) cell lines (U87-MG, U251, U373) were used to study their mutual paracrine interactions in the indirect co-cultures compared to their monocultures, which were grown under the same experimental conditions. The effects on cell growth, proliferation and invasion in matrigel were quantified. Further on, bioinformatic tools were used to relate these results to the data obtained from cytokine macroarrays and DNA microarrays that revealed proteins and genes significantly involved in the interaction. We showed that hMSC are responsible for the impairment of GBM cell invasion and growth, possibly via induction of their senescence. On the other hand, U87-MG cells even more strongly inversely affected some of these characteristics in hMSCs. We found several chemokines that may account for changed co-cultured cells’ phenotype, affecting genes associated with proliferation and senescence. CCL2/MCP-1 was collectively identified as the most significantly regulated chemokine during hMSC and U87-MG paracrine signalling. Its role in U87-MG cell invasion was also functionally confirmed. Microarray data deposited here contain gene expression data from three biological replicates of monocultures and indirect co-cultures of MSC-4 and U87-MG cells, representing 12 microarrays. Three biological replicates of four cell set-ups were performed: MSC-4 monoculture, U87-MG monoculture, MSC-4 co-cultured with U87-MG (in Boyden chambers) and U87-MG co-cultured with MSC-4 (in Boyden chambers).

2011-12-20 | E-GEOD-26283 | biostudies-arrayexpress

Human Mesenchymal Stem Cells Exploit the Immune Response Mediating Chemokines to Impact the Phenotype of Glioblastoma

2011-12-20 | GSE26283 | GEO

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

Project description: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

2018-05-01 | GSE106159 | GEO

The RNA polymerase II subunit B gene(POLR2B) functions as a growth regulator in human glioblastoma

Project description:Glioblastoma multiform (GBM) is the most common and aggressive brain tumor with dismissal prognosis. POLR2B encodes the second largest subunit of the RNA polymerase II, but its genomic status and function in GBM remains unclear. To explore POLR2B-dependent gene regulation, RNA-seq analysis was performed. Compared with the control group, POLR2B knockdown DBTRG-05MG cells showed differently expressed genes.

2022-11-10 | GSE192823 | GEO

Dual IRE1 RNase functions dictate glioblastoma development

Project description:The transcriptome dataset has been used to validate on a GBM patient cohort (n=117) the IRE1-dependent gene expression signature identified in U87 cell line.

2018-01-09 | E-MTAB-6326 | biostudies-arrayexpress

Discovery of PDE7B as a novel effector of GBM growth by computational deconvolution of an in vitro physical coculture system

Project description:Cell-to-cell interactions between tumor cells and their microenvironment are critical determinants of tumor tissue biology and therapeutic responses. Interactions between glioblastoma (GBM) cells and endothelial cells (ECs) establish a purported stem cell niche. We hypothesized that genes that mediate these interactions would be important, particularly as therapeutic targets. Using a novel computational approach to deconvoluting expression data from mixed physical coculture of GBM cells and ECs, we identified upregulation of the cAMP specific phosphodiesterase PDE7B in GBM cells in response to ECs. We further found that elevated PDE7B expression occurs in most GBM cases and has a negative effect on survival. PDE7B overexpression resulted in the expansion of a stem-like cell subpopulation, increased tumor aggressiveness, and increased growth in an intracranial GBM model. This deconvolution algorithm provides a new tool for cancer biology, and these results identify PDE7B as a therapeutic target in GBM. 3 replicates from U87 monocultures, 3 replicates from HBMEC monocultures, 3 replicates from U87-HBMEC cocultures

2014-03-01 | E-GEOD-51253 | biostudies-arrayexpress

Allopregnanolone alters the gene expression profile of human glioblastoma cells

Project description:Glioblastomas (GBM) are one of the most frequent and aggressive brain tumors. In these malignancies, progesterone (P4) promotes proliferation, migration, and invasion. The P4 metabolite allopregnanolone (3α-THP) similarly promotes cell proliferation in the U87 human GBM cell line. Here, we evaluated global changes in gene expression of U87 cells treated with 3α-THP, P4, and the 5α-reductase inhibitor, finasteride (F).

2018-02-11 | GSE108998 | GEO

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