Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic reprogramming in hepatic carcinogenesis

ABSTRACT: Epigenetic reprogramming in hepatic carcinogenesis

PROVIDER: PRJNA450821 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7029650.fastq.gz	Fastqsanger.gz
	SRR7029651.fastq.gz	Fastqsanger.gz
	SRR7029652.fastq.gz	Fastqsanger.gz
	SRR7029653.fastq.gz	Fastqsanger.gz
	SRR7029654.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming

Project description:Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming

| PRJNA507535 | ENA

Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming [RNA-seq]

Project description:Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming [RNA-seq]

| PRJNA507539 | ENA

Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming [ChIP-seq]

Project description:Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming [ChIP-seq]

| PRJNA507538 | ENA

Epigenetic reprogramming in hepatic carcinogenesis

2018-07-02 | GSE113326 | GEO

Dynamic changes in the epigenetic landscape are mandatory for acinar cell reprogramming and pancreatic carcinogenesis [ChIP-seq]

Project description:Pancreatic acinar cell reprogramming is described as a common hallmark in pancreatic regeneration and carcinogenesis, although the regulatory mechanisms are barely understood. To overcome limitations of cellular diversity posed by heterogeneous cell compositions and high stroma density in pathogenic tissue specimens, we have established a pure in vitro system mimicking the pancreatic carcinogenic sequence. With this model, we globally profiled for epigenetic and transcriptional alterations and demonstrate that regulatory key players and structural genes are extensively regulated by epigenetic mechanisms. A conditional knockout of the epigenetic repressor Ring1b showed that particularly the epigenetic silencing of acinar differentiation genes is a crucial step in acinar cell reprogramming and pancreatic cancer development. Moreover, a persistent epigenetic repression of these genes manifests tumor cell malignancy. Depletion or drug-dependent inhibition of Ring1b promoted tumor cell reprogramming towards a less aggressive phenotype offering new options for therapeutic intervention.

2019-04-23 | GSE116151 | GEO

Dynamic changes in the epigenetic landscape are mandatory for acinar cell reprogramming and pancreatic carcinogenesis [microarray]

2019-04-23 | GSE116150 | GEO

Loss of tumor suppressor IGFBP4 drives epigenetic reprogramming in hepatic carcinogenesis.

Project description:Genomic sequencing of hepatocellular carcinoma (HCC) uncovers a paucity of actionable mutations, underscoring the necessity to exploit epigenetic vulnerabilities for therapeutics. In HCC, EZH2-mediated H3K27me3 represents a major oncogenic chromatin modification, but how it modulates the therapeutic vulnerability of signaling pathways remains unknown. Here, we show EZH2 acts antagonistically to AKT signaling in maintaining H3K27 methylome through epigenetic silencing of IGFBP4. ChIP-seq revealed enrichment of Ezh2/H3K27me3 at silenced loci in HBx-transgenic mouse-derived HCCs, including Igfbp4 whose down-regulation significantly correlated with EZH2 overexpression and poor survivals of HCC patients. Functional characterizations demonstrated potent growth- and invasion-suppressive functions of IGFBP4, which was associated with transcriptomic alterations leading to deregulation of multiple signaling pathways. Mechanistically, IGFBP4 stimulated AKT/EZH2 phosphorylation to abrogate H3K27me3-mediated silencing, forming a reciprocal feedback loop that suppressed core transcription factor networks (FOXA1/HNF1A/HNF4A/KLF9/NR1H4) for normal liver homeostasis. Consequently, the in vivo tumorigenicity of IGFBP4-silenced HCC cells was vulnerable to pharmacological inhibition of EZH2, but not AKT. Our study unveils chromatin regulation of a novel liver tumor suppressor IGFBP4, which constitutes an AKT-EZH2 reciprocal loop in driving H3K27me3-mediated epigenetic reprogramming. Defining the aberrant chromatin landscape of HCC sheds light into the mechanistic basis of effective EZH2-targeted inhibition.

| S-EPMC6158508 | biostudies-literature

Hepatic expression data from 2-stage carcinogenesis study in rats

Project description:Hepatic gene expression profiles in 2-stage carcinogenesis study were analyzed with comprehensive DNA methylation data. Combined analysis suggested that PTEN signaling and immune response such as antigen presentation was related to one side of early heapatocarcinogenesis. We used microarrays to obtain the global gene expression profile of livers to understand the mechanism of carcinogenesis.

2016-10-24 | GSE51797 | GEO

Transcription profiling of rodent hepatic carcinogenesis

Project description:3 dose levels of each of 9 compounds were used to dose male SD rats q.d. by oral gavage. Compounds included 5 nongenotoxic carcinogens (bemitradine, clofibrate, doxylamine, methapyrilene, & phenobarbital), 2 genotoxic agents (tamoxifen and 2-AAF) and 2 non-carcinogens (4-AAF and isoniazid). This work has been described in Kramer JA, Curtiss SW, Kolaja KL, Alden CA, Blomme EAG, Curtiss WC, Davila JC, Jackson CJ, and Bunch RT. (2004) Acute Molecular Markers of Rodent Hepatic Carcinogenesis Identified by Transcription Profiling. Chem. Res. Toxicol., in press.

2004-03-08 | E-MEXP-89 | biostudies-arrayexpress

Dynamic changes in the epigenetic landscape are mandatory for acinar cell reprogramming and pancreatic carcinogenesis

Project description:Dynamic changes in the epigenetic landscape are mandatory for acinar cell reprogramming and pancreatic carcinogenesis

| PRJNA477452 | ENA