Chromatin Profiling of SD48 bladder cancer cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE193880 | GEO | 2023/03/22
REPOSITORIES: GEO
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Project description:In order to investigate epigenetic landscape and potential alterations in bladder, we established the chromatin profiling of 5637 cell line by ChIPseq for the following marks and transcription factor : H3K4me3, H3K9ac, H3K27me3, H3K9me3, H3K27ac, H3K4me1, CTCF and FOXA1.
2023-03-22 | GSE193811 | GEO
Project description:Tumor progression is related to both genetic and epigenetic alterations. Until relatively recently, epigenetic changes were thought to target single genes only but we show that in Bladder tumours, epigenetic changes can affect whole chromosomal regions, resulting in the silencing of all the genes within those regions. This phenomenon is probably very general, and has been described in bladder, colon, breast and prostate cancers. In order to investigate epigenetic landscape and potential alterations in bladder, we established the chromatin profiling of RT112 cell line by ChIPseq for the following marks : H3K4me3, H3K9ac, H3K27me3, H3K9me3, H3K27ac, H3K4me1, and CTCF.
2023-03-22 | GSE140891 | GEO
Project description:Tumor progression is related to both genetic and epigenetic alterations. Until relatively recently, epigenetic changes were thought to target single genes only but we show that in Bladder tumours, epigenetic changes can affect whole chromosomal regions, resulting in the silencing of all the genes within those regions. This phenomenon is probably very general, and has been described in bladder, colon, breast and prostate cancers. In order to investigate epigenetic landscape and potential alterations in bladder, we established the chromatin profiling of RT112 cell line by ChIPseq for the following marks : H3K4me3, H3K9ac, H3K27me3, H3K9me3, H3K27ac, H3K4me1, and CTCF.
2023-03-22 | GSE104804 | GEO
Project description:<p>The primary goal of this study was to collect and analyze genomic data from primary glioblastoma multiforme tumors. Our collaborators at St David's Medical Center (SDMC) obtained informed consent from patients undergoing surgery to remove a tumor in the brain. After consent was obtained, specimens were removed from the operating suite and flash frozen in liquid nitrogen. Tumors were analyzed if they were a grade III (anaplastic astrocytoma) or grade IV glioma (glioblastoma multiforme). Tumors were transported from SDMC to UT Austin, then weighed and homogenized. Chromatin immunoprecipitation was performed for 7 proteins in each tumor (histone modifications H3K4me3, H3K4me1, H3K9ac, H3K9me3, H3K27ac, H3K27me3, and the multifunctional insulator binding protein CTCF) and no-antibody input was also sequenced. An aliquot of tumor material was set aside for isolation of total RNA.</p>
| phs001389 | dbGaP
Project description:Sequence data of 28 Samples (19 chronic lymphocytic leukemia, 9 control)
Including RNA-Seq and ChIP-Seq of following histone modifications: H3, H3K4me1, H3K4me3, H3K9ac, H3K9me3, H3K27ac, H3K27me3, H3K36me3
Project see: http://www.cancerepisys.org/
| EGAD00001003421 | EGA
Project description:Provide a first characterization of the chromatin landscapes of bladder cancers. Using ChIPseq (H3K27ac, H3K27me3, H3K9me3) in tumors characterized at the genetic, DNA methylation and transcriptomic levels, we will identify active regulatory regions. We will in particular define the super-enhancers active in the different molecular subtypes recently described.
2023-03-22 | GSE193889 | GEO
Project description:FOXA1 is a pioneer factor that is important in hormone dependent cancer cells to stabilise nuclear receptors, such as estrogen receptor (ER) to chromatin. FOXA1 binds to enhancers regions that are enriched in H3K4mono- and dimethylation (H3K4me1, H3K4me2) histone marks and evidence suggests that these marks are requisite events for FOXA1 to associate with enhancers to initate subsequent gene expression events. However, exogenous expression of FOXA1 has been shown to induce H3K4me1 and H3K4me2 signal at enhancer elements and the order of events and the functional importance of these events is not clear. We performed a FOXA1 Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins (RIME) screen in ERα-positive MCF-7 breast cancer cells in order to identify FOXA1 interacting partners and we found histone-lysine N-methyltransferase (MLL3) as the top FOXA1 interacting protein. MLL3 is typically thought to induce H3K4me3 at promoter regions, but recent findings suggest it may contribute to H3K4me1 deposition, in line with our observation that MLL3 associates with an enhancer specific protein. We performed MLL3 ChIP-seq in breast cancer cells and unexpectedly found that MLL3 binds mostly at non-promoter regions enhancers, in contrast to the prevailing hypothesis. MLL3 was shown to occupy regions marked by FOXA1 occupancy and as expected, H3K4me1 and H3K4me2. MLL3 binding was dependent on FOXA1, indicating that FOXA1 recruits MLL3 to chromatin. Motif analysis and subsequent genomic mapping revealed a role for Grainy head like protein-2 (GRHL2) which was shown to co-occupy regions of the chromatin with MLL3. Regions occupied by all three factors, namely FOXA1, MLL3 and GRHL2, were most enriched in H3K4me1. MLL3 silencing decreased H3K4me1 at enhancer elements, but had no appreciable impact on H3K4me3 at enhancer elements. We identify a complex relationship between FOXA1, MLL3 and H3K4me1 at enhancers in breast cancer and propose a mechanism whereby the pioneer factor FOXA1 can interact with a chromatin modifier MLL3, recruiting it to chromatin to facilitate the deposition of H3K4me1 histone marks, subsequently demarcating active enhancer elements.
2016-12-12 | PXD005253 | Pride
Project description:ChIPseq data for human glioblastoma patients, EGAS00001003953. Mix of input, H3K27ac, H3K27me1, H3K27me3, H3K36me3, H3K4me1, H3K4me3, H3K9me3 and BRD, 20 human samples, 2 cell lines (LN229, ZH487).
| EGAD00001006548 | EGA
Project description:This study aims to investigate the DNA methylation patterns at transcription factor binding regions and their evolutionary conservation with respect to binding activity divergence. We combined newly generated bisulfite-sequencing experiments in livers of five mammals (human, macaque, mouse, rat and dog) and matched publicly available ChIP-sequencing data for five transcription factors (CEBPA, HNF4a, CTCF, ONECUT1 and FOXA1). To study the chromatin contexts of TF binding subjected to distinct evolutionary pressures, we integrated publicly available active promoter, active enhancer and primed enhancer calls determined by profiling genome wide patterns of H3K27ac, H3K4me3 and H3K4me1.
2022-10-20 | E-MTAB-11946 | biostudies-arrayexpress
Project description:Background: Muscle-invasive bladder cancer is a common aggressive disease with unmet clinical needs. Recent work established a set of consensus bladder cancer transcriptomic subtypes that distinguishes the cell identity of bladder cancers for improved diagnosis and treatment. However, how these distinct subtypes are regulated remains unclear. Given the link between super-enhancers and the regulation of cell identity, we hypothesized that epigenetic activation of distinct super-enhancers could drive the transcriptional programs of the various bladder cancer subtypes. Results: Through integrated RNA sequencing and epigenomic profiling of histone marks (H3K27ac, H3K27me3, H3K9me3) in a diverse panel of 15 primary bladder tumours, seven bladder cancer cell lines, and two primary cultures from normal human urothelia, we established the first integrated epigenetic map of bladder cancer and demonstrate the link between bladder cancer subtype and epigenetic control. Through H3K27ac analysis, we identify the repertoire of activated super-enhancers in bladder cancer that distinguish molecular subtypes. Building on these findings, we reveal the super-enhancer-regulated networks of candidate master transcription factors for Luminal and Basal bladder cancer subgroups. We find that FOXA1, a key pioneer factor in Luminal bladder cancers identified in our Luminal transcription factor network, binds subgroup-specific bladder super-enhancers and correlates with their activation. Furthermore, CRISPR-Cas9 inactivating mutation of FOXA1 triggers a shift from Luminal to Basal cell identity. This shift is accompanied by an overexpression of ZBED2, one of the newly identified transcriptional regulators in the Basal-specific transcription factor network. 5Finally, we show that both FOXA1 and ZBED2 play concordant roles in preventing inflammatory response in bladder cancer cells through STAT2 inhibition and promote cancer cell survival. Conclusions: Overall, our study provides new data for understanding epigenetic regulation of muscle- invasive bladder cancer and identifies a coregulated network of super-enhancers and associated transcription factors as new potential targets for the treatment of this aggressive disease
2024-05-23 | GSE195768 | GEO