To examine the role of p300 in the SMARCA4–p53 regulatory axis, we performed ChIP-seq to assess p300, p53, H3K27ac, HDAC1, HDAC2 occupancy in BIN-67 cells
Ontology highlight
ABSTRACT:
INSTRUMENT(S): NextSeq 500
ORGANISM(S): Homo sapiens
SUBMITTER: Giulio Aceto
PROVIDER: E-MTAB-15700 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We aim to test how SMARCA4 restoration impacts p300 occupancy distribution. To this aim we generated ChIP-seq samples in BIN-67 with or without A-485 treatment (1 μM, 24h), as a proxy for p300 acetylatransferase inhibition, and BIN-67 with inducible SMARCA4 restoration (1 μg/ml Doxycycline for 24h). We pulled down p300 and H3K27ac as a marker for p300 acetyltransferase activity on the chromatin.
2026-05-05 | E-MTAB-15699 | biostudies-arrayexpress
Project description:To examine the role SMARCA4-p53 regulatory axis in SCCOHT cells we performed RNA-seq in BIN-67 cells with SMARCA4 restoration, p53ko alone or combined with SMARCA4 and idasanutlin treatment (0.5μM, 24h) which increase the stability of p53 and its protein levels in SCCOHT.
2026-05-05 | E-MTAB-15707 | biostudies-arrayexpress
Project description:RNA-seq samples in BIN-67 and BIN-67p53-ko cells with or without A-485 treatment (1μM, 24h). The goal of the experiment is to assess the genes that are regulated by p300 acetyltransferase inhibition using A-485 treatment and weather p53-ko can rescue this phenotype.
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Project description:RNA-seq samples in BIN-67, COV434, SCCOHT-1 cells including Control (Ctrl.) and A-485 treatment (24h, 1μM)
2026-05-05 | E-MTAB-15705 | biostudies-arrayexpress
Project description:RNA-seq samples in SCCOHT-1 and COV434 for idasanutlin treatment (0.5μM, 24h), and RNA-seq samples in BIN-67 and COV434 for short-term idasanutlin treatment (0.5μM, 3h). The goal of the experiment is to assess the genes that are regulated by p53 stabilization in the long term or short term using idasanutlin treatment in SCCOHT.
2026-05-05 | E-MTAB-16956 | biostudies-arrayexpress
Project description:The biology of small cell ovarian carcinoma of the hypercalcemic type (SCCOHT), which is a rare and aggressive form of ovarian cancer, is poorly understood. Tumourigenicity, in vitro growth characteristics, genetic and genomic anomalies, and sensitivity to standard and novel chemotherapeutic treatments were investigated in the unique SCCOHT cell line, BIN-67, to provide further insight in the biology of this rare type of ovarian cancer. Chromosomal anomalies in BIN-67 cells were inferred using the Infinium? genotyping technology with the HumanHap300-Duo Genotyping BeadChip (Illumina, San Diego, CA, USA). This BeadChip contains about 318,000 genetic markers within approximately a 5 kb median SNP spacing. Genotyping and imaging using BeadStudio Data Analysis software (Illumina, San Diego, CA, USA) were performed at the McGill University and Genome Quebec Innovation Centre (Montreal, QC).
2013-09-24 | E-MTAB-1584 | biostudies-arrayexpress
Project description:The biology of small cell ovarian carcinoma of the hypercalcemic type (SCCOHT), which is a rare and aggressive form of ovarian cancer, is poorly understood. Tumourigenicity, in vitro growth characteristics, genetic and genomic anomalies, and sensitivity to standard and novel chemotherapeutic treatments were investigated in the unique SCCOHT cell line, BIN-67, to provide further insight in the biology of this rare type of ovarian cancer. Microarray expression analysis was performed using the GeneChip? Human Genome U133 Plus 2.0 Array (Affymetrix?, Santa Clara, CA) with total RNA from BIN-67 cells. Hybridization and scanning were performed at the McGill University and Genome Quebec Innovation Centre (Montreal, QC). Gene expression levels were determined from the scanned images using Affymetrix? Microarray Suite (MAS) version 5.0 software expression algorithm (Affymetrix?, Santa Clara, CA). Gene expression profiles were compared with Affymetrix U133 Plus 2.0 (MAS5.0) generated expression profiles (similarly normalized) from 10 human normal ovarian surface epithelial (OSE) cell brushings available in the ArrayExpress database (www.ebi.ac.uk/arrayexpress/), accession number E-GEOD-18520.
2013-09-24 | E-MEXP-3872 | biostudies-arrayexpress
Project description:Purpose: The purpose of this study was to develop a framework for analyzing RPE expression profiles from zebrafish eye mutants. Methods: The fish model we used was smarca4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4), a retinal dystrophic mutant that the retinal phenotype and expression profiles were previously characterized. Histological and Affymetrix GeneChip analyses were conducted to define the RPE defects and underlying differential expression respectively. Results: Histological analysis indicates that smarca4 RPE was formed but its differentiation was abnormal. In particular, ultra-structural analysis of smarca4 RPE by transmission electron microscopy showed a number of defects in melanogenesis, suggesting that the cytoskeletal dynamics was impaired. To compare the expression profile of normal wild-type (WT) and smarca4 RPE, their retinas and RPE-attached retinas were microdissected and the gene expression values of these tissues measured by Affymetrix GeneChip analysis. The RPE expression values were then estimated from these samples using an approach previously established by us. A factorial analysis was conducted using the expression values of RPE, retinal as well as the whole-embryo samples. Specific rules (contrasts) were built using the coefficients of the resulting fitted model to select for three groups of genes: 1) Smarca4-regulated RPE genes, 2) Smarca4-regulated retinal genes, and 3) Smarca4-regulated RPE genes that are not differentially expressed in the retina. The latter group consists of 39 genes that are highly related to cytoskeletal dynamics, melanogenesis, paracrine and intracellular signal transduction. Conclusions: Our analytical framework can potentially identify genes in zebrafish mutants that both retina and RPE are affected by the underlying mutation. The gene expression levels of three independent replicates of WT whole embryos (WA52), WT retinas (WR52), WT RPE-attached retinas (WRR52), smarca4/yng retinas (YR52), smarca4 RPE-attached retinas (YRR52) and smarca4 whole embryos (YA52) were measured by Affymetrix Zebrafish Whole Genome Arrays. All samples were collected at 52 hpf. The probe-level data of these sample groups were background adjusted, normalized and summarized by a robust multiarray average (RMA) algorithm. RPE expression values were estimated from the comparison between the retinal and RPE-attached retinal samples of the same genotype based on a method we previously developed (Leung et al., Invest Ophthalmol Vis Sci. 2007; 48:881). Then, a 3x2 factorial design was used to analyze the expression values of three kinds of tissue (T): whole embryo, retina and RPE in two kinds of mutation (M) background: WT and smarca4. Using the coefficients from the fitted models, contrasts were built to identify candidate genes that fulfilled specific criteria. The false discovery rate (FDR) q-value cutoff for a contrast was 0.001. Several contrasts were ultimately combined to allow for selection of genes that were regulated by Smarca4 in the retina and RPE. These include 1) Smarca4-regulated RPE genes, 2) Smarca4-regulated retinal genes, and 3) Smarca4-regulated RPE genes that are not differentially expressed in the retina.
2014-01-03 | E-GEOD-50241 | biostudies-arrayexpress
Project description:Assessing SMARCA4 restoration contribution to global changes in p300 occupancy in BIN-67 cells
| PRJEB98942 | ENA
Project description:Cyclin-Dependent Kinase 9 (CDK9) as part of the PTEFb complex promotes transcriptional elongation by promoting RNAPII pause release. We now report that, paradoxically, CDK9 is also essential for maintaining gene silencing at heterochromatic loci. Through a live cell screen, we discovered that CDK9 inhibition reactivates epigenetically silenced genes in cancer, leading to restored tumor suppressor gene expression and cell differentiation, along with activation of endogenous retrovirus (ERV) genes. CDK9 inhibition dephosphorylates the SWI/SNF protein SMARCA4 and represses HP1α expression, both of which contribute to gene reactivation. Based on gene activation, we developed the highly selective and potent CDK9 inhibitor MC180295 (IC50 =5nM) that has broad anti-cancer activity in-vitro and is effective in in-vivo cancer models. Additionally, CDK9 inhibition sensitizes with the immune checkpoint inhibitor α-PD-1 in vivo, making it an excellent target for epigenetic therapy of cancer.
2020-05-26 | PXD009573 | Pride