Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-site CpG Profiling for KMT2D and HNF4A genomic region in pancreatic cancer cells.

ABSTRACT: Differential CpG methylation profiling for KMT2D and HNF4A genomic region in pancreatic cancer cells was performed using Illumina MiSeq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE85961 | GEO | 2018/08/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [Cut&Tag]

Project description:CUT-Tag revealed a strong reduction of KMT2D, H3K4me1 and EBF2 signals at the transcription start site (TSS) and promoter regions of genes that were downregulated in KMT2D-depleted (KMT2D-KD) cells

2023-07-18 | GSE237365 | GEO

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]

Project description:ChIP-seq revealed a strong reduction of KMT2D, H3K4me1 and EBF2 signals at the transcription start site (TSS) and promoter regions of genes that were downregulated in KMT2D-depleted (KMT2D-KD) cells

2023-07-18 | GSE237364 | GEO

KMT2D Links TGF-β Signalling to Non-Canonical Activin Pathway and Regulates Pancreatic Cancer Cell Plasticity

Project description:Although KMT2D, also known as MLL2, is known to play an essential role in development, differentiation, and tumor suppression, its role in pancreatic cancer development is not well understood. Here, we discovered a novel signaling axis mediated by KMT2D, which links TGF-β to the activin A pathway. We found that TGF-β upregulates a microRNA, miR-147b, which in turn leads to post-transcriptional silencing of KMT2D. Loss of KMT2D induces the expression and secretion of activin A, which activates a non-canonical p38 MAPK-mediated pathway to modulate cancer cell plasticity, promote a mesenchymal phenotype, and enhance tumor invasion and metastasis in mice. We observed a decreased KMT2D expression in human primary and metastatic pancreatic cancer. Furthermore, inhibition or knockdown of activin A reversed the pro-tumoral role of KMT2D loss. These findings support a tumor-suppressive role of KMT2D in pancreatic cancer and identify miR-147b and activin A as novel therapeutic targets.

2023-03-31 | GSE199856 | GEO

Aberrant downstream mechanisms following loss of KMT2C and KMT2D in Pancreatic Ductal Adenocarcinoma

Project description:Genes encoding the histone H3 lysine 4 (H3K4) methyltransferases KMT2C and KMT2D are subject to deletion and mutation in pancreatic ductal adenocarcinomas (PDAC). We examined the functional and transcriptional consequences of loss of these methyltransferases in patients with PDAC. Patients with low KMT2C and KMT2D expression demonstrated a much-improved outcome compared with those expressing high levels. RNA-seq analysis of KMT2C or KMT2D loss in three cell lines (PANC1, SUIT2 and COLO357) identified 31 and 124 differentially expressed genes respectively, with 19 genes common to both methlytransferases. Gene set enrichment analysis, and correlation with publicly available patient gene expression (GEP) datasets, highlighted significant reductions in pathways relating to cell-cycle and cell growth, where gene expression correlated with KMT2C/D depletion. Furthermore, loss of Kmt2d in three murine cell lines increased sensitivity to the nucleoside analogue 5-fluorouracil (5FU). These experiments support critical, non-redundant, roles for KMT2D and KMT2C in PDAC, where depletion impacts cell-cycle to reduce cell proliferation, enhance response to specific chemotherapy, which may improve patient survival.

2016-07-09 | GSE75327 | GEO

CpG underrepresentation and the new bacterial CpG specific DNA methyltransferase M.MpeI

Project description:The CpG depleted Mycoplasma penetrans harbors a CpG specific C5 methyltransferase. The aim of this experiment was to confirm the specificity of the methyltransferase in vivo and in vitro. Genomic DNA from Mycoplasma penetrans and Escherichia coli genomic DNA that either was or was not methylated in vitro by M.MpeI were subjected to Illumina MiSeq bisulfite sequencing.

2012-11-29 | E-GEOD-41022 | biostudies-arrayexpress

H3K4me2 and gene expression profiling in control and KMT2D KD murine B220 cells

Project description:Define and compare H3K4me2 enrichment in murine B220 cells transduced with empty vector (ct) or KMT2D-shRNA. Compare gene expression by RNAseq in murine B220 cells transduced with empty vector (ct) or KMT2D-shRNA. Using H3K4me1/2 ChIPseq and RNAseq we profiled murine B220 purified cells from tumors transduced with EV (n=3) or KMT2D-shRNA (n=3).

2015-08-28 | E-GEOD-67291 | biostudies-arrayexpress

RNA-seq of KMT2D Knockout and KMT2D WT melanoma in mice

Project description:Somatic mutations in various epigenetic regulators, including histone methyltransferases KMT2C and KMT2D, have emerged as important cancer-driving events. However, the mechanism of action and therapeutic vulnerability imparted by these mutations remain poorly understood. We identified KMT2D and 8 other epigenetic regulators as potential suppressors to melanoma initiation through an in vivo pooled epigenome-focused RNAi screen. Loss of KMT2D, which exhibits somatic mutations in human melanoma and other cancers, drastically enhanced melanoma progression in xenograft models and a BRAFV600E-driven genetically engineered mouse model of melanoma. Epigenome profiling of 6 histone marks and chromatin state alterations showed substantial reprogramming of H3K4me1- and H3K27ac-marked active enhancer states in KMT2D mutant tumors. Energy metabolic pathways such as glycolysis, OxPhos and TCA/electron transport showed high degree of deregulation which was confirmed with metabolic profiling. Pharmacological abrogation of glycolysis led to reduced proliferation and tumorigenesis preferentially in KMT2D mutant cells. Mechanistically, we find that enhancer loss at IGFBPs increases IGF signaling and downstream AKT phosphorylation that leads to upregulation of metabolic pathways rendering KMT2D mutant cells dependent on these energy metabolism pathways for their higher growth potential. Overall, we present evidence that KMT2D mutations promote tumorigenesis by reprogramming energy metabolism pathways through enhancer reprogramming.

2020-11-16 | GSE116852 | GEO

Hnf4a regulated transcriptome

Project description:Hnf4a regulated transcriptome

| PRJNA574921 | ENA

Effect of loss of HNF4A in liver and effect of ectopic expression of HNF4A in mouse fibroblast cells

Project description:To understand how HNF4A loss affects gene expression in mouse liver. We used control and HNF4A KO mouse livers for RNA sequencing. In addition, we also examined the effect of HNF4A gain in mouse fibroblast cells by ectropically expressing HNF4A in NIH3T3 cell to identify genes that are regulated by HNF4A.

2024-01-15 | GSE210842 | GEO

Analysis of transcriptome changes in Kmt2d deletion in cardiac mesoderm, anterior heart field precursors and cardiomyocytes

Project description:KMT2D is required in the cardiac mesoderm, anterior heart field precursors and cardiomyocytes. Kmt2d deletion in cardiac mesoderm (Mesp1Cre) is embryonic lethal at E10.5 and mutants have hypoplastic hearts; Kmt2d deletion in anterior heart field precursors (Mef2cAHF::Cre) deletion is embryonic lethal at E13.5 and mutants have defects in septation of outflow tract and interventricular septum (IVS); Kmt2d deletion in cardiomyocytes (Tnnt2::Cre) deletion is embryonic lethal at E14.5 and mutants have defects in IVS septation and compact myocardium. The goal of this study is to compare changes in gene expression in these Kmt2d conditional deletion mutants and understand common or distinct pathways dysregulated in absence of KMT2D. Whole genome gene expression analysis was performed on RNA isolated from control and mutant embryonic hearts (or right ventricles and outflow tract for anterior heart field deletion samples). Libraries were prepared using Illumina TruSeq Paired-End Cluster Kit v3, and sequenced with the Illumina HiSeq 2500 system for pair-ended 100 base pairs (PE 100 bp).

2015-11-04 | E-GEOD-74679 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data