Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Low KLF11 Determines the CSC–like Identity in Sarcoma via restraining YAP transactivity [ATAC-seq]

ABSTRACT: We conducted Transposase-accessible chromatin using sequencing (ATAC-seq) experiments to compare chromatin open regions between control and KLF11-knockdown cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE133311 | GEO | 2020/06/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Low KLF11 Determines the CSC–like Identity in Sarcoma via restraining YAP transactivity [RNA-seq]

Project description:We conducted transcriptome comparison of control and KLF11-knockdown MG63 cells.

2020-06-25 | GSE133309 | GEO

Low KLF11 Determines the CSC–like Identity in Sarcoma via restraining YAP transactivity [ChIP-seq]

Project description:We conducted ChIP-seq experiments to investigate the role of KLF11 in YAP/TEAD transcriptional activity.

2020-06-25 | GSE133310 | GEO

Low KLF11 Determines the CSC–like Identity in Sarcoma via restraining YAP transactivity

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-25 | GSE133312 | GEO

Browning of human adipocytes requires KLF11 and reprogramming of PPARγ super-enhancers

Project description:Here we have characterized the transcriptional processes underlying the formation of human brown in white (i.e. brite) adipocytes using a genome-wide approach. We show that the browning process is associated with reprogramming of peroxisome proliferator-activated receptor γ (PPARγ) binding to form brite adipocyte-selective PPARγ super-enhancers that appear to play a key role in activation of brite adipocyte-selective genes. We identify the KLF11 gene based on its association with a PPARγ super-enhancer and show that KLF11 is a novel browning factor directly induced by rosiglitazone and required for the activation of brite adipocyte-selective gene program by rosiglitazone. Genome-wide profiling of Dnase I hypersenstive (DHS) sites, epigenomic marks, transcription factor and co-factor binding, and gene expression in hMADS white and brite adipocytes

2014-12-12 | E-GEOD-59703 | biostudies-arrayexpress

Browning of human adipocytes requires KLF11 and reprogramming of PPARγ super-enhancers

2014-12-12 | GSE59703 | GEO

Expression data from Panc1 pancreatic epithelial cells

Project description:KrÃ¼ppel-like factors (KLFs) are a group of master regulators of gene expression conserved from flies to human. However, scant information is available on either the mechanisms or functional impact of the coupling of KLF proteins to chromatin remodeling machines, a deterministic step in transcriptional regulation. In the current study, we use genome-wide analyses of chromatin immunoprecipitation (ChIP-on-Chip) and Affymetrix-based expression profiling to gain insight into how the KLF11, a human transcription factor involved in tumor suppression and metabolic diseases, works by coupling to three co-factor groups: the Sin3-histone deacetylase system, WD40-domain containing proteins, and the HP1-histone methyltransferase system. We utilized genome-wide expression analysis of wild type KLF11 and three mutants that disrupt KLF11-chromatin machinery interactions to examine the relationship of the transcription factor and chromatin systems in the regulation of gene networks. Panc1 epithelial cells were plated at a density of 1x10^6 cells/100mm dish and transduced with empty vector, KLF11, KLF11-A347S, KLF11-486, or KLF11-EAPP adenovirus at an MOI of 150. RNA was prepared as previously described from pooled biological triplicates.

2014-08-01 | E-GEOD-56778 | biostudies-arrayexpress

Transcriptome analysis of human aortic endothelial cells (HAECs) with KLF11 knockdown

Project description:Transcriptome analysis of human aortic endothelial cells (HAECs) with KLF11 knockdown

| PRJNA639465 | ENA

Fructose-1,6-Bisphosphatase 2 Inhibits Sarcoma Progression by Restraining Mitochondrial Biogenesis.

Project description:The remarkable cellular and genetic heterogeneity of soft tissue sarcomas (STSs) limits the clinical benefit of targeted therapies. Here, we show that expression of the gluconeogenic isozyme fructose-1,6-bisphosphatase 2 (FBP2) is silenced in a broad spectrum of sarcoma subtypes, revealing an apparent common metabolic feature shared by diverse STSs. Enforced FBP2 expression inhibits sarcoma cell and tumor growth through two distinct mechanisms. First, cytosolic FBP2 antagonizes elevated glycolysis associated with the "Warburg effect," thereby inhibiting sarcoma cell proliferation. Second, nuclear-localized FBP2 restrains mitochondrial biogenesis and respiration in a catalytic-activity-independent manner by inhibiting the expression of nuclear respiratory factor and mitochondrial transcription factor A (TFAM). Specifically, nuclear FBP2 colocalizes with the c-Myc transcription factor at the TFAM locus and represses c-Myc-dependent TFAM expression. This unique dual function of FBP2 provides a rationale for its selective suppression in STSs, identifying a potential metabolic vulnerability of this malignancy and possible therapeutic target.

| S-EPMC6949384 | biostudies-literature

PPARγ agonists promote differentiation of cancer stem cells by restraining YAP transcriptional activity.

Project description:Osteosarcoma (OS) is a highly aggressive pediatric bone cancer in which most tumor cells remain immature and fail to differentiate into bone-forming osteoblasts. However, OS cells readily respond to adipogenic stimuli suggesting they retain mesenchymal stem cell-like properties. Here we demonstrate that nuclear receptor PPARγ agonists such as the anti-diabetic, thiazolidinedione (TZD) drugs induce growth arrest and cause adipogenic differentiation in human, mouse and canine OS cells as well as in tumors in mice. Gene expression analysis reveals that TZDs induce lipid metabolism pathways while suppressing targets of the Hippo-YAP pathway, Wnt signaling and cancer-related proliferation pathways. Significantly, TZD action appears to be restricted to the high Sox2 expressing cancer stem cell population and is dependent on PPARγ expression. TZDs also affect growth and cell fate by causing the cytoplasmic sequestration of the transcription factors SOX2 and YAP that are required for tumorigenicity. Finally, we identify a TZD-regulated gene signature based on Wnt/Hippo target genes and PPARγ that predicts patient outcomes. Together, this work highlights a novel connection between PPARγ agonist in inducing adipogenesis and mimicking the tumor suppressive hippo pathway. It also illustrates the potential of drug repurposing for TZD-based differentiation therapy for osteosarcoma.

| S-EPMC5308629 | biostudies-literature

YAP-Driven Malignant Reprogramming of Oral Epithelial Stem Cells, ATAC sequencing

Project description:Assay for Transposase Accessible Chromatin (ATAC) sequencing of tongue epithelia-derived, transgene-selected primarily cultured cells from control mice or transgenic mice expressing HPV16E6-E7 and YAP1S127A

2024-09-09 | GSE276778 | GEO

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