Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lung adenocarcinoma UNC0638 gene expression

ABSTRACT: Experiment was to determine the effects of G9a inhibition using chemical inhibitor UNC0638 on murine lung adenocarcinoma cell lines

ORGANISM(S): Mus musculus

PROVIDER: GSE120073 | GEO | 2018/09/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Lung adenocarcinoma UNC0638 gene expression

Project description:Lung adenocarcinoma UNC0638 gene expression

| PRJNA491480 | ENA

G9a-dependent gene expression in mouse AML cells

Project description:The methyltransferase G9a was found to play a role in the disease progression of a murine model of AML. Mouse HSPCs were transformed with HoxA9/Meis1 and treated with G9a/GLP inhibitor UNC0638. We used microarrays to detail the global program of gene expression that depends on the methyltransferase activity of G9a in murine AML cells.

2014-01-08 | E-GEOD-53894 | biostudies-arrayexpress

G9a-dependent gene expression in mouse AML cells

2014-01-08 | GSE53894 | GEO

Epithelial signatures of chemical-induced lung adenocarcinoma

Project description:Epithelial signatures of chemical-induced lung adenocarcinoma

| PRJNA375075 | ENA

Chromatin changes in G9a inhibited lung adenocarcinoma cells

Project description:Chromatin changes in G9a inhibited lung adenocarcinoma cells

| PRJNA451516 | ENA

Expression data from G9a overexpression and knockdown lung cancer cell lines

Project description:G9a is the major mammalian H3-K9 methyltransferase that targets euchromatic regionsand is essential for murine embryogenesis . We demonstrate that G9a is endowed with methyltransferase activity to concomitantly repress the downstream effector Ep-CAM, thereby promoting the invasion step of the invasion-metastasis cascade. We used microarrays to detail the G9a regulated gene expression underlying invasion-metastasis cascade and identified distinct classes of up-regulated genes during this process. Lung adenocarcinoma cells with G9a knockdown or overexpression were selected for RNA extraction and hybridization on Affymetrix microarrays.

2011-12-31 | E-GEOD-22810 | biostudies-arrayexpress

H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression

Project description:We have identified the histone methyltransferases G9a/Glp as suppressors of aggressive lung tumor-propagating cells (TPCs). Chemically inhibiting G9a/Glp promoted TPC phenotypes in lung adenocarcinoma cells, and caused chromatin changes at genes associated with the differentiation of stem cells. G9a/Glp inhibition in lung progenitor cell organoid cultures disrupted alveolar differentiation. Depleting G9a during tumorigenesis enriched for TPCs, accelerating disease progression and metastasis. Demethylase inhibition decreased lung adenocarcinoma progression in vivo.

2018-11-30 | GSE100455 | GEO

H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression (experiment 2)

2021-04-19 | GSE113402 | GEO

Inhibition of H3K9me2-specific histone methyltransferase, G9a/GLP, reveals transcripts regulated by the establishment of H3K9me2 in hematopoietic stem and progenitor cells

Project description:We have performed RNA-seq from DMSO control treated, G9a/GLP inhibitor (UNC0638) treated, and DNA-demethylating agent (Decitabine) treated CD34+ hematopoietic stem and progenitor cells. This experiment was performed to identify transcripts that were uniquely affected by the loss of H3K9me2 in hematopoietic stem and progenitor cells.

2023-05-01 | GSE204743 | GEO

Ito2019 - gefitnib resistance of lung adenocarcinoma caused by MET amplification

Project description:The model is based on publication: Mathematical analysis of gefitinib resistance of lung adenocarcinoma caused by MET amplification Abstract: Gefitinib, one of the tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR), is effective for treating lung adenocarcinoma harboring EGFR mutation; but later, most cases acquire a resistance to gefitinib. One of the mechanisms conferring gefitinib resistance to lung adenocarcinoma is the amplification of the MET gene, which is observed in 5–22% of gefitinib-resistant tumors. A previous study suggested that MET amplification could cause gefitinib resistance by driving ErbB3-dependent activation of the PI3K pathway. In this study, we built a mathematical model of gefitinib resistance caused by MET amplification using lung adenocarcinoma HCC827-GR (gefitinib resistant) cells. The molecular reactions involved in gefitinib resistance consisted of dimerization and phosphorylation of three molecules, EGFR, ErbB3, and MET were described by a series of ordinary differential equations. To perform a computer simulation, we quantified each molecule on the cell surface using flow cytometry and estimated unknown parameters by dimensional analysis. Our simulation showed that the number of active ErbB3 molecules is around a hundred-fold smaller than that of active MET molecules. Limited contribution of ErbB3 in gefitinib resistance by MET amplification is also demonstrated using HCC827-GR cells in culture experiments. Our mathematical model provides a quantitative understanding of the molecular reactions underlying drug resistance.

2019-09-30 | BIOMD0000000827 | BioModels

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