Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting WNT Signaling for Improved Glioma Immunotherapy [PBT]

ABSTRACT: Metabolic gene expression analysis to explore ICG-001’s impact on metabolic changes associated with glioma differentiation after disrupting the CBP/β-Catenin interaction by treating patient-derived GBM cell lines PBT147 and PBT030 with ICG-001 (0, 5, or 10 µM) for 24 and 72 h using Nanostring nCounter platform

ORGANISM(S): Homo sapiens

PROVIDER: GSE252155 | GEO | 2024/02/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The Î²-catenin/CBP-antagonist ICG-001 inhibits pediatric glioma tumorigenicity in a Wnt-independent manner

Project description:In pediatric glioma cell lines, treatment with ICG-001 had no inhibitory effect on canonical Wnt-target genes but induced significant up regulation of various known Î²-catenin target genes in both cell lines and top 20 GO-annotations of down-regulated genes by ICG-001 were associated with biosynthetic and metabolic processes and cell cycle division processes. Pediatric cell lines were treated with ICG-001 or DMSO for 48h

2016-06-14 | E-GEOD-83266 | biostudies-arrayexpress

The β-catenin/CBP-antagonist ICG-001 inhibits pediatric glioma tumorigenicity in a Wnt-independent manner

Project description:In pediatric glioma cell lines, treatment with ICG-001 had no inhibitory effect on canonical Wnt-target genes but induced significant up regulation of various known β-catenin target genes in both cell lines and top 20 GO-annotations of down-regulated genes by ICG-001 were associated with biosynthetic and metabolic processes and cell cycle division processes.

2016-06-14 | GSE83266 | GEO

Altering cancer transcriptomes using epigenomic inhibitors [Illumina beadchip]

Project description:We have compared the genome-wide effects on the transcriptome after treatment with ICG-001 (the specific CBP inhibitor) versus C646, a compound that competes with acetyl-coA for the Lys-coA binding pocket of both CBP and p300. We found that both drugs cause large-scale changes in the transcriptome of HCT116 colon cancer cells and PANC1 pancreatic cancer cells, and reverse some tumor-specific changes in gene expression. Interestingly, although the epigenetic inhibitors affect cell cycle pathways in both the colon and pancreatic cancer cell lines, the WNT signaling pathway was affected only in the colon cancer cells. Notably, WNT target genes were similarly down-regulated after treatment of HCT116 with C646 as with ICG-001. Total RNA obtained from isolated HCT116 or PANC1 cell lines were treated with 10uM ICG-001, 10uM C646, or 0.05% DMSO and collected after 12 or 96 hours.

2015-01-07 | E-GEOD-64038 | biostudies-arrayexpress

RNA-seq in HSJD-DIPG-007 cells treated with JQ1, ICG-001, JQ1 and ICG-001 and DMSO as control.

Project description:This study aims to characterize gene expression changes upon treatment with JQ1, ICG-001, and combined treatment. The general goal is to identify the mechanism for high efficacy of combinatorial treatment of BET and CBP inhibition in DIPG cells.

2020-08-01 | E-MTAB-8243 | biostudies-arrayexpress

Altering cancer transcriptomes using epigenomic inhibitors [Illumina beadchip]

2015-01-07 | GSE64038 | GEO

Altering cancer transcriptomes using epigenomic inhibitors [RNA-Seq]

2015-01-07 | GSE63776 | GEO

Altering cancer transcriptomes using epigenomic inhibitors [RNA-Seq]

Project description:We have compared the genome-wide effects on the transcriptome after treatment with ICG-001 (the specific CBP inhibitor) versus C646, a compound that competes with acetyl-coA for the Lys-coA binding pocket of both CBP and p300. We found that both drugs cause large-scale changes in the transcriptome of HCT116 colon cancer cells and PANC1 pancreatic cancer cells, and reverse some tumor-specific changes in gene expression. Interestingly, although the epigenetic inhibitors affect cell cycle pathways in both the colon and pancreatic cancer cell lines, the WNT signaling pathway was affected only in the colon cancer cells. Notably, WNT target genes were similarly down-regulated after treatment of HCT116 with C646 as with ICG-001. To identify genes affected by direct targeting of a component of the transcriptional complex implicated in WNT regulation, we used siRNAs to knockdown TCF7L2 in PANC1 cells. Cells were treated with control siRNAs or siRNAs specific for TCF7L2 and RNA was analyzed by RNA-seq.

2015-01-07 | E-GEOD-63776 | biostudies-arrayexpress

Regulation of gene expression in uveal melanoma cells by ICG-001

Project description:We examined the effects of ICG-001 on gene expression in Mel202 uveal melanoma (UM) cells. ICG-001 exerted strong antiproliferative activity against UM cells, leading to cell cycle arrest, apoptosis, and inhibition of migration. Global gene expression profiling revealed strong suppression of genes associated with cell cycle proliferation, DNA replication, and G1/S transition. Gene set enrichment analysis revealed that ICG-001 suppressed Wnt, mTOR, and MAPK signaling. Strikingly, ICG-001 suppressed the expression of genes associated with UM aggressiveness, including CDH1, CITED1, EMP1, EMP3, SDCBP, and SPARC. Notably, the transcriptomic footprint of ICG-001, when applied to a UM patient dataset, was associated with better clinical outcome. Lastly, ICG-001 exerted anticancer activity against a UM tumor xenograft in mice.

2020-04-28 | GSE149417 | GEO

ICG-001 activates a series of ER stress response genes in monocyte derived macrophages (MDMs)

Project description:By screening a target-focused Wnt-sgnaling small compound library we identified the Wnt-modulator ICG-001 as inihibitory for activating the mitochondrial fission protein Drp1. To explore how ICG-001 might act we undertook gene expression profiling in iCG-001 treated primary macrophages.

2018-01-12 | GSE102117 | GEO

Targeting oncogenic β-catenin/CBP activity for the treatment of head and neck squamous cell carcinoma

Project description:Head and neck squamous cell carcinoma (HNSCC) presents primarily as oral squamous cell carcinoma (OSCC), an aggressive malignancy characterized by heterogeneity, locoregional metastases and resistance to existing treatments. Although a number of molecular alterations associated with OSCC have been identified, they have had limited impact on clinical management. A frequent feature of OSCC is the inappropriate activation of nuclear β-catenin. Here, we provide a comprehensive characterization of the effects of blocking the interaction between nuclear β-catenin and the cAMP-responsive element binding (CREB)-binding protein (CBP) using the small molecule inhibitor ICG-001. We demonstrate that ICG-001 inhibits cell proliferation and aggressive OSCC cell phenotypes in cellular, zebrafish and murine models, and that its inhibition-associated transcriptional signature tracks with advanced tumor grade and poor survival in human patients. Our results suggest that targeting the β-catenin/CBP interaction in the nucleus represents a new and effective therapy for OSCC.

2018-07-03 | GSE95704 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data