Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

ABSTRACT: GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

OTHER RELATED OMICS DATASETS IN: GSE111305

PROVIDER: PRJNA436558 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

Project description:Ovarian cancer (OC) cells frequently metastasize to the omentum and adipocytes play a significant role in ovarian tumor progression. Therapeutic interventions targeting aberrant DNA methylation in ovarian tumors have shown promise in the clinic but the effects of epigenetic therapy on the tumor microenvironment are understudied. Here, we examined the effect of adipocytes on OC cell behavior in culture and impact of targeting DNA methylation in adipocytes on OC metastasis. The presence of adipocytes increased OC cell migration and invasion and proximal and direct co-culture of adipocytes .increased OC proliferation alone or after treatment with carboplatin. Treatment of adipocytes with hypomethylating agent guadecitabine decreased migration and invasion of OC cells towards adipocytes. Due to this result, we performed RNA-seq of adipocytes treated with DNMT1 inhibitor to analyze differential gene expression changes that occur in the adipocyte that may explain the above observation that hypomethylating agent treatment of adipocytes decrease migration and invasion.

2018-03-02 | GSE111305 | GEO

DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

Project description:DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

| PRJNA437571 | ENA

DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

2018-03-10 | GSE111617 | GEO

Genome-wide maps of Dnmt1-dependent DNA methylome in adipocytes

Project description:White adipose tissue (WAT) is a key regulator of systemic energy metabolism, and impaired WAT plasticity characterized by enlargement of preexisting adipocytes associates with WAT dysfunction, obesity and metabolic complications. However, the mechanisms that retain proper adipose tissue plasticity required for metabolic fitness are unclear. Here, we comprehensively showed that adipocyte-specific DNA methylation, manifested in enhancers and CTCF sites, directs distal enhancer-mediated transcriptomic features required to conserve metabolic functions of white adipocytes. Particularly, genetic ablation of adipocyte Dnmt1, the major methylation writer, led to increased adiposity characterized by increased adipocyte hypertrophy along with reduced expansion of adipocyte precursors (APs). These effects of Dnmt1 deficiency provoked systemic hyperlipidemia and impaired energy metabolism both in lean and obese mice. Mechanistically, Dnmt1 deficiency abrogated mitochondrial bioenergetics by inhibiting mitochondrial fission and promoted aberrant lipid metabolism in adipocytes, rendering adipocyte hypertrophy and WAT dysfunction. Dnmt1-dependent DNA methylation prevented aberrant CTCF binding and, in turn, sustained the proper chromosome architecture to permit interactions between enhancer and dynamin-related protein gene Drp1 in adipocytes. Also, adipose DNMT1 expression inversely correlated with adiposity and markers of metabolic health, but positively correlated with AP-specific markers in obese human subjects. Thus, these findings support strategies utilizing Dnmt1 action on mitochondrial bioenergetics in adipocytes to combat obesity and related metabolic pathology.

2021-03-24 | GSE158944 | GEO

Epigenetic Interaction between UTX and DNMT1 in brown adipocytes

Project description:Epigenetic Interaction between UTX and DNMT1 in brown adipocytes

| PRJNA733054 | ENA

Genome-wide maps of Dnmt1-dependent DNA methylome in adipocytes

Project description:Genome-wide maps of Dnmt1-dependent DNA methylome in adipocytes

| PRJNA667071 | ENA

Refractory testicular germ cell tumors are highly sensitive to the second generation DNA methlation inhibitor guadecitabine

Project description:Comparison of gene expression in cisplatin resistant testicular germ cell tumor xenografts treated with vehicle (PBS) or the DNA methylation inhibitor guadecitabine

2017-01-01 | GSE90681 | GEO

The DNMT1 inhibitor GSK-3484862 mediates global demethylation in murine embryonic stem cells

Project description:We generated WGBS datasets from mESCs treated with the novel drug GSK-3484862 attained from two different commercial sources or the conventional DNMT1 inhitibitor 5-azacytidine. To assess efficacy, datasets were generated from mESCs treated with GSK-3484862 at two concentrations and after treatment for 6 days and 14 days each. Additionally, for comparison purposes, we generated WGBS datasets from Dnmt1/3a/3b deficient mESCs which have very low levels of DNA methylation and WT mESCs treated with DMSO which retain high levels of DNA methylation.

2021-12-14 | GSE184116 | GEO

Genomic and epigenomic predictors of response to Guadecitabine in relapsed/refractory Acute Myelogenous Leukemia

Project description:Guadecitabine is a second generation DNA methylation inhibitor with improved pharmacokinetics and clinical activity in relapsed/refractory AML (rrAML). Here we report genome-wide DNA methylation profiles in pre-treatment samples from 116 rrAML patients treated at therapeutic doses of guadecitabine in a phase I/II study. Response rate to guadecitabine was 22 % (16CR, 42 12CRi/CRp). There were no strong mutation or methylation predictors of response. Gene expression defined a subset of patients (~20%) that had (i) high DNMT3B and low CDKN2B, CTCF and CDA expression, (ii) enrichment for KRAS/NRAS mutations, (iii) frequent CpG island hypermethylation (iv) low LINE1 hypomethylation after treatment and (v) resistance to guadecitabine in both phase I (response rate 0 % vs 33 %, p=0.07) and phase II components of the study (response rate 5 % vs. 30 %, p=0.02). Multivariate analysis identified peripheral blood blasts and hemoglobin as predictors of response and cytogenetics, gene expression, RAS mutations and hemoglobin as predictors of survival. Thus, a subset of patients (∿ 20%) with rrAML are unlikely to benefit from single agent guadecitabine. In the remaining 80%, guadecitabine is a viable option with a median survival of ∿ 8 months and a three year survival rate of over 20%.

2019-08-06 | GSE112838 | GEO

Gene expression signatures in 3T3-L1 adipocytes 2, 8 and 20 days after the induction of adipocyte differentiation

Project description:To identify the genes that increase in hypertrophic adipocytes, we have performed DNA microarray analysis in 3T3-L1 adipocytes. Hypertrophic adipocytes were obtained by long-term culture in routine cell culture medium. 2, 8 and 20 days after the induction of adipogenesis, total RNA was isolated.

2020-04-01 | GSE147858 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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