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Nanoscale Chromatin Profiling of Gastric Adenocarcinoma

ABSTRACT: To identify chromatin alterations in primary gastric adenocarcionomas, we performed nano-scale chromatin immunoprecipitation-sequencing (Nano-CHiPseq) of histone modifications in 5 gastric cancers and matched normal tissues, We identified hundreds of somatically-altered promoters (marked by H3K4me3) and enhancers (H3K4me1). The majority of cancer-associated promoters localized to genomic sites lacking previously-annotated transcription start sites (“cryptic promoters”), driving high expression of nearby genes implicated in gastrointestinal cancers, embryonic development, and tissue specification. Our findings demonstrate the feasibility of performing chromatin profiling on solid tumors where tissue is limiting, to identify in non-coding regions regulatory elements, transcriptional patterns and genetic variants associated with cancer. We propose a pervasive role for cryptic promoters in the reactivation of early developmental programs in gastric cancer, and the potential utility of cryptic promoters as biomarkers of malignancy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51776 | GEO | 2014/07/30

SECONDARY ACCESSION(S): PRJNA225015

REPOSITORIES: GEO

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Nanoscale Chromatin Profiling of Gastric Adenocarcinoma

Project description:To identify chromatin alterations in primary gastric adenocarcionomas, we performed nano-scale chromatin immunoprecipitation-sequencing (Nano-CHiPseq) of histone modifications in 5 gastric cancers and matched normal tissues, We identified hundreds of somatically-altered promoters (marked by H3K4me3) and enhancers (H3K4me1). The majority of cancer-associated promoters localized to genomic sites lacking previously-annotated transcription start sites (“cryptic promoters”), driving high expression of nearby genes implicated in gastrointestinal cancers, embryonic development, and tissue specification. Our findings demonstrate the feasibility of performing chromatin profiling on solid tumors where tissue is limiting, to identify in non-coding regions regulatory elements, transcriptional patterns and genetic variants associated with cancer. We propose a pervasive role for cryptic promoters in the reactivation of early developmental programs in gastric cancer, and the potential utility of cryptic promoters as biomarkers of malignancy. Five gastric cancer tumor normal pairs are profiling in multiple number of chromatin marks

2014-07-30 | E-GEOD-51776 | biostudies-arrayexpress

Methylation Analysis of Gastric Cancers

Project description:Examine methylation changes in gene promoters in gastric cancers and matched normal control gastric epithelium, using Nimblegen arrays. Direct comparison of gastric cancers and matched normal control gastric epithelium

2013-06-14 | E-GEOD-40919 | biostudies-arrayexpress

A non-canonical SWI/SNF complex underlies synthetic lethality in cancers driven by BAF complex perturbation

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2018-11-06 | PXD011103 | Pride

Widespread transposable element-driven oncogene expression in cancers

Project description:Transposable elements act as promiscuous cryptic promoters that upregulate oncogenes (“onco-exaptation”) in many cancers.

2019-02-05 | GSE113946 | GEO

ChIP-DSL H20K promoter array from human gastric cancer cells MKN28 with Sox2 overexpression

Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes. Transcription factor Sox2 promoter array in MKN28 cells with Sox2 overexpression.

2013-05-22 | E-GEOD-45427 | biostudies-arrayexpress

Chromatin-dependent cryptic promoters encode alternative protein isoforms in yeast

Project description:Cryptic transcription is widespread and generates a heterogeneous group of RNA molecules of unknown function. To improve our understanding of cryptic transcription, we investigated their transcription start site usage, chromatin organization and post-transcriptional consequences in Saccharomyces cerevisiae. We show that transcription start sites of chromatin-dependent internal cryptic transcripts resemble those of protein coding genes in terms of DNA sequence, directionality and chromatin accessibility. We define the 5’ and 3’ boundaries of cryptic transcripts and show that, contrary to RNA degradation-dependent ones , they often overlap with the end of the gene thereby using the canonical polyadenylation site and associate to polyribosomes. In fact, we show that chromatin-dependent cryptic transcripts can be recognized by ribosomes and may produce truncated polypeptides from downstream, in-frame start codons. Our work suggests that a significant fraction of chromatin-dependent internal cryptic promoters are in fact alternative truncated mRNA isoforms. The expression of these chromatin-dependent isoforms is conserved from yeast to human expanding the functional consequences of cryptic transcription and proteome complexity.

2019-10-01 | GSE119114 | GEO

Identification of non-coding transcripts regulated by the transcription factor Rap1 by RNA-Seq analysis

Project description:Many active eukaryotic gene promoters exhibit divergent noncoding transcription, but the mechanisms restricting expression of these transcripts are not well understood. Here we demonstrate how a sequence-specific transcription factor represses divergent noncoding transcription at highly expressed genes in yeast. We find that depletion of the transcription factor Rap1 induces noncoding transcription in a large fraction of Rap1 regulated gene promoters. Specifically, Rap1 prevents transcription initiation at cryptic promoters near its binding sites, which is uncoupled from transcription regulation in the protein-coding direction. We further provide evidence that Rap1 acts independently of chromatin-based mechanisms to repress cryptic or divergent transcription. Finally, we show that divergent transcription in the absence of Rap1 is elicited by the RSC chromatin remodeller. We propose that a sequence-specific transcription factor limits access of basal transcription machinery to regulatory elements and adjacent sequences that act as divergent cryptic promoters, thereby providing directionality towards productive transcription.

2018-12-20 | GSE107813 | GEO

Somatic mouse models of gastric cancer reveal genotype-specific features of metastatic disease

Project description:Metastatic gastric carcinoma is a highly lethal cancer that responds poorly to conventional and molecularly targeted therapies. Despite its clinical relevance, the mechanisms underlying the behavior and therapeutic response of this disease are poorly understood owing, in part, to a paucity of tractable models that faithfully recapitulate different subtypes of the human disease. To close this gap, we developed methods to somatically introduce different oncogenic lesions directly into the stomach epithelium and show that genotypic configurations observed in patients produce metastatic gastric cancers that recapitulate the histological, molecular, and clinical features of all non-viral molecular subtypes of the human disease. Applying this platform to both wild-type and immune-deficient mice revealed previously unappreciated links between the genotype, organotropism and immune surveillance of metastatic cells that produced distinct patterns of metastasis that were mirrored in patients. Our results establish and credential a highly portable platform for producing autochthonous cancer models with flexible genotypes and host backgrounds, which can unravel mechanisms of gastric tumorigenesis or test new therapeutic concepts aimed at improving outcomes in gastric cancer patients.

2023-09-03 | GSE199261 | GEO

Methylation Analysis of Gastric Cancers

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2013-06-14 | GSE40919 | GEO

ChIP-seq data for Cbp1 and CreN7 in Saccharolobus solfataricus P2

Project description:Chromatin proteins competes with the transcription machinery for access to genomic DNA and suppress cryptic promoters. CRISPR arrays form the physical memory of CRISPR adaptive immune systems. The incorporation of virus-derived AT-rich DNA into CRISPR arrays renders them prone to harbouring cryptic promoters. Sulfolobales feature extremely long CRISPR arrays spanning several kilobases as well as a CRISPR-specific chromatin protein termed Cbp1. Altered Cbp1 expression affects transcription from CRISPR arrays in multiple ways, but the mechanistic basis remains to be understood. Here, we show that Cbp1 recruits the general chromatin protein Cren7 to form a heteromeric chromatin complex at CRISPR arrays. Cbp1-CreN7 chromatinisation plays a dual role in the transcription of CRISPR array. It suppresses spurious transcription from cryptic CRISPR array-internal promoters via steric occlusion of the transcription machinery while enhancing transcription from promoters in the CRISPR leaders. Our results show that Cbp1-CreN7 chromatinization drives the coordinated transcription of long CRISPR arrays. Additional binding sites of Cbp1 associated with transposases and the leaders of alternative CRISPR arrays hint on a wider regulatory function of Cbp1 linking defense systems and mobile genetic elements.

2023-03-24 | GSE226025 | GEO

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