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Expression data from AsPC1 cells treated with ICG-001

ABSTRACT: The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin) AsPC1 cells were treated with 10uM ICG-001 or vehicle control (DMSO) for either 6 hours or 24 hours. AsPC-1 cells were also separately transfected with 20nM control siRNA or CTNNB1 siRNA for 48 hours. RNA was extracted at these time points for hybridization to Affymetrix microarrays

ORGANISM(S): Homo sapiens

SUBMITTER: David Dawson

PROVIDER: E-GEOD-57728 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The CREB-binding protein inhibitor ICG-001 suppresses pancreatic cancer growth.

Arensman Michael D MD Telesca Donatello D Lay Anna R AR Kershaw Kathleen M KM Wu Nanping N Donahue Timothy R TR Dawson David W DW

Molecular cancer therapeutics 20140731 10

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer due in part to a lack of highly robust cytotoxic or molecular-based therapies. Recent studies investigating ligand-mediated Wnt/β-catenin signaling have highlighted its importance in pancreatic cancer initiation and progression, as well as its potential as a therapeutic target in PDAC. The small-molecule ICG-001 binds cAMP-responsive element binding (CREB)-binding protein (CBP) to disrupt its interaction with β-catenin and inhibit ...[more]

PMID: 25082960

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Expression data from AsPC1 cells treated with ICG-001

Project description:The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin)

2014-07-15 | GSE57728 | GEO

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

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

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]

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