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Genome-wide profiling of siRNA targeting PRKDC in Ewing sarcoma and non-Ewing sarcoma cell lines

ABSTRACT: Identification of genes and pathways that were influenced by knock-down PRKDC in TC32 Ewing sarcoma and HCT116 colorectal carcinoma cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE93075 | GEO | 2018/08/03

REPOSITORIES: GEO

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Genome-wide profiling of siRNA targeting EWS-FLI1 in TC32 Ewing sarcoma cell line

Project description:Identification of genes and pathways that were influenced by knock-down EWS-FLI1 in TC32 Ewing sarcoma cell line.

2018-09-05 | GSE103843 | GEO

Genome-wide profiling of Ewing sarcoma cell lines with nu7441 treatment

Project description:Identification of genes and pathways that were influenced by nu7441, the PRKDC inhibitor, in Ewing sarcoma cell lines.

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Expression profiling of the TC32 Ewing sarcoma cell line following silencing of SUPT6H, SF3B1 or HNRNPH1

Project description:The investigation of the function of SUPT6H, SF3B1 and HNRNPH1 in Ewing sarcoma The expression profiles of TC32 Ewing sarcoma cells were determine 48 hours post siRNA-transfected. Groups consisted of untreated cells (three samples), and negative control (siNeg) transfected-TC32 cells (six samples), and TC32 cells in which either SUPT6H, SF3B1 or HNRNPH1 were silenced; three different siRNAs corresponding to each gene were assessed separately.

2016-01-15 | E-GEOD-67736 | biostudies-arrayexpress

Ewing Sarcoma cell lines treated with mithramycin

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Enriched EWSR1 and EWS-FLI1 RNA-seq of HNRNPH1-silenced TC32 Ewing sarcoma and 293T human embryonic kidney cells.

Project description:Identification of EWSR1 and EWS-FLI1 transcript variants associated with the silencing of HNRNPH1 in TC32 Ewing sarcoma and 293T human embryonic kidney (HEK-293T) cells.

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Expression profiling of Ewing sarcoma cell lines exposed to 5nM Pladienolide B (PlaB) for 24 hours

Project description:Identification of genes and pathways altered by PlaB, a bacterial natural product that acts as a spliceosome modulator by targeting the SF3b subunit of the spliceosome SKNMC, TC32, TC71, and RD-ES Ewing sarcoma cell lines were treated with 0.1% (v/v) DMSO vehicle or 5nM PlaB for 24 hours. Three samples in each group were analyzed.

2016-01-15 | E-GEOD-67548 | biostudies-arrayexpress

Wnt/beta-catenin activated Ewing sarcoma cells promote the angiogenic switch

Project description:Wnt/beta-catenin signaling is active in small subpopulations of Ewing sarcoma cells and these cells display a more metastatic phenotype, in part due to antagonism of EWS-FLI1-dependent transcriptional activity. Importantly, these beta-catenin-activated Ewing cells also alter secretion of extracellular matrix (ECM) proteins. We thus hypothesized that, in addition to cell autonomous mechanisms, Wnt/beta-catenin-active tumor cells might contribute to disease progression by altering the tumor microenvironment (TME). Activation of canonical Wnt signaling leads Ewing sarcoma cells to upregulate expression and secretion of pro-angiogenic ECM proteins, collectively termed the angiomatrix. Here we tested the role of Wnt-related TGF-beta signaling in angiomatrix induction by obtaining mRNA from Wnt3a-treated TC32 cells in the presence and absence of SB505124, a chemical inhibitor of TGF-beta receptor 1 (TGFBR1) and subjecting it to short read RNA-sequencing.

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Targeting EWSR1-FLI1 oncogene induced protein kinase C beta abolishes Ewing sarcoma growth in vivo

Project description:Identification of druggable targets is a prerequisite for developing targeted therapies against Ewing sarcoma. We report the identification of Protein Kinase C Beta (PRKCB) as a protein specifically and highly expressed in Ewing sarcoma as compared to other pediatric cancers. Its transcriptional activation is directly regulated by the EWSR1-FLI1 oncogene. Getting insights in PRKCB activity we show that, together with PRKCA, it is responsible for the phosphorylation of histone H3T6, allowing global maintenance of H3K4 trimethylation on a variety of gene promoters. In the long term, PRKCB RNA interference induces apoptosis in vitro. More importantly, in xenograft mice models, complete impairment of tumor engraftment and even tumor regression were observed upon PRKCB inhibition, highlighting PRKCB as a most valuable therapeutic target. Deciphering PRKCB roles in Ewing sarcoma using expression profiling, we found a strong overlap with genes modulated by EWSR1-FLI1 and an involvement of RPKCB in regulating crucial signaling pathways. Altogether, we show that PRKCB may have two important independent functions and should be considered as highly valuable for understanding Ewing sarcoma biology and as a promising target for new therapeutic approaches in Ewing sarcoma. A673 Ewing cell line was treated for 72 hours by either control siRNA or siRNA directed against PRKCB or EWSR1-FLI1. Total RNAs were extracted and hybridized on HuGene1.1STv1 Affymetrix Arrays. Normalisation was performed using specific Brainarray Enrtez gene CDF file (v14.1).

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Ewing Sarcoma

Project description:This SuperSeries is composed of the following subset Series: GSE36857: Goldengate Methylation analysis: Ewing Sarcoma GSE36858: 5- AZA treatment of EWS cell lines Refer to individual Series

2012-09-01 | E-GEOD-36859 | biostudies-arrayexpress

RUNX3 Facilitates Growth of Ewing Sarcoma Cells

Project description:Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA

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