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Links from GEO DataSets

Items: 20

1.

Epigenomic profiling of Non-small-cell Lung Cancer (NSCLC) cells with or without Eed

(Submitter supplied) Polycomb repressive complexes (PRC) are frequently implicated in human cancer acting either as oncogenes or tumor suppressors. Here we show that PRC2 is a critical regulator of Kras-driven non-small-cell lung cancer (NSCLC) progression. Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances Kras-driven adenomagenesis and inflammation, respectively. Eed-loss-driven inflammation leads to massive macrophage recruitment and marked decline in tissue function. more...
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL17021 GPL16791
31 Samples
Download data: BED, BIGWIG, BW, TXT
Series
Accession:
GSE61190
ID:
200061190
2.

Transcriptional and Epigenomic profile of GSK126 or dox-mediated Ezh2 inhibition in KrasG12D/+;Trp53-/-;Ezh2i-GFP-2A-rTA;Luc lung tumors in vivo

(Submitter supplied) We wanted to understand the consequences of GSK126-mediated Ezh2 inhibition in an orthotopic model of Kras-driven non-small cell lung cancer (NSCLC). We injected the NSCLC cells with above-mentioned genotype into Nude mice and treated them with GSK126 50mg/kg (daily) or vehicle. As additional control for Ezh2 specificity we treated one tumor with doxycycline that induces shRNA-mediated Ezh2 protein downregulation in those cells. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL13112
18 Samples
Download data: BW, TXT
Series
Accession:
GSE61125
ID:
200061125
3.

Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2

(Submitter supplied) Adenosquamous lung tumors may result from cellular plasticity. We demonstrate lineage switching of KRAS+ lung adenocarcinomas (ADC) to squamous cell carcinoma (SCC) through deletion of Lkb1 (Stk11) in autochthonous and transplant models. Chromatin analysis reveals loss of H3K27me3 and gain of H3K27ac and H3K4me3 at squamous lineage genes, included Sox2, ΔNp63 and Ngfr. SCC lesions have higher levels of the H3K27 methyltransferase EZH2 than the ADC lesions, but there is a clear lack of the essential Polycomb Repressive Complex 2 (PRC2) subunit EED in the SCC lesions.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: BED, WIG
Series
Accession:
GSE94365
ID:
200094365
4.

Gene expression profiling of Eed knockout and Ezh2 knockout small intestinal crypts

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL13112
18 Samples
Download data: BIGWIG
Series
Accession:
GSE81578
ID:
200081578
5.

Gene expression profiling of Eed knockout and Ezh2 knockout small intestinal crypts [ChIP-seq]

(Submitter supplied) Polycomb-mediated gene repression plays an important role in adult stem cell maintenance. Direct targets of the Polycomb repressive complex PRC2 in th intestinal epithelium were revealed by performing ChIP-sequencing on crypt samples isolated from wild type murine small intestines. The resulting list of H3K27me3-enriched genes were compared with RNA-sequencing data from wild type and Eed knockout crypts.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
5 Samples
Download data: BIGWIG
Series
Accession:
GSE81577
ID:
200081577
6.

Gene expression profiling of Eed knockout and Ezh2 knockout small intestinal crypts [RNA-seq]

(Submitter supplied) Polycomb-mediated gene repression plays an important role in adult stem cell maintenance. We knocked out (using the inducible AhCre-LoxP system) Polycomb genes Eed and Ezh2 in the intestine for 6 weeks, after which crypts - the small intestinal stem cell zone - were harvested and RNA sequenced. We found Wnt, Notch and cell cycle pathways to be affected in Eed knockout (KO) but not Ezh2 KO crypts. Direct targets of Eed were determined by comparing this data with ChIP-sequencing.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL13112
13 Samples
Download data: TXT
Series
Accession:
GSE81576
ID:
200081576
7.

Chip-seq analysis of H3K4me3, H3K27me3, DNMT1 and EZH2 binding to chromatin following acute (10 days) and chronic (10 months) treatment of human bronchial epithelial cells (HBEC3KT) cells with 10 µg/ml cigarette smoke condensate (CSC).

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
20 Samples
Download data: BED
Series
Accession:
GSE103331
ID:
200103331
8.

Exome-seq analysis of human bronchial epithelial cells (HBEC3KT) cells pre and post treatment with DMSO (Control) or 10 µg/ml cigarette smoke condensate (CSC) for 15 months and tumor xenografts obtained with 15 month CSC treated cells expressing KRASV12

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Other
Platforms:
GPL15520 GPL16791
10 Samples
Download data
Series
Accession:
GSE103150
ID:
200103150
9.

Chronic Cigarette Smoke-Induced Epigenomic, gene expression and chromatin changes in Bronchial Epithelial Cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array; Expression profiling by array; Other; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
86 Samples
Download data: BED, IDAT, PDF, TXT
Series
Accession:
GSE101864
ID:
200101864
10.

Gene Expression of HBEC-3KT cells exposed to cigarette smoke condensate (CSC) over a period of 15 months

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10332
16 Samples
Download data: PDF, TXT
Series
Accession:
GSE101863
ID:
200101863
11.

Genes expression in xenografts obtained from 15 months cigarette smoke condensate (CSC)-exposed HBEC cells following expression of KRASV12

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10332
9 Samples
Download data: PDF, TXT
Series
Accession:
GSE101862
ID:
200101862
12.

Methylation analysis of HBEC cells exposed to cigarette smoke condensate (CSC) over a period of 15 months

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
31 Samples
Download data: IDAT, TXT
Series
Accession:
GSE101673
ID:
200101673
13.

Polycomb Deficiency Drives a FOXP2-high Metastatic State Targetable by Epigenetic Inhibitors

(Submitter supplied) The purpose of this research is to understand the role and expand the precision medicine of EZH2 inhibition in lung adenocarcinoma. Our data show that histone methyltransferase EZH2 acts in a context-dependent manner as an oncogene or tumor suppressor in KRAS+/Trp53-null murine lung adenocarcinoma. Moreover, EZH2 deprivation confers sensitivity to histone demethylase and BET inhibitors in 3D culture and in vivo models, representing precision medicine strategies for lung cancers with low canonical EZH2 activity. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
7 Samples
Download data: BED
Series
Accession:
GSE182819
ID:
200182819
14.

Polycomb Deficiency Drives a FOXP2-high Aggressive State Targetable by Epigenetic Inhibitors

(Submitter supplied) The purpose of this research is to understand the role and expand the precision medicine of EZH2 inhibition in lung adenocarcinoma. Our data show that histone methyltransferase EZH2 acts in a context-dependent manner as an oncogene or tumor suppressor in KRAS+/Trp53-null murine lung adenocarcinoma. Moreover, EZH2 deprivation confers sensitivity to histone demethylase and BET inhibitors in 3D culture and in vivo models, representing precision medicine strategies for lung cancers with low canonical EZH2 activity. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
99 Samples
Download data: TXT
Series
Accession:
GSE154689
ID:
200154689
15.

Loss of histone demethylase KDM6B enhances aggressiveness of pancreatic cancer through downregulation of C/EBPα

(Submitter supplied) Genetic mutations in pancreatic ductal adenocarcinoma (PDAC) with critical roles have been well examined. The recent discovery of alterations in genes encoding histone modifiers suggests their possible roles in the complexity of cancer development. We previously reported loss of heterozygosity of the KDM6B gene, which encodes a histone demethylase for trimethylated histone H3 lysine 27 (H3K27me3), a repressive chromatin mark, in PDAC cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6480
6 Samples
Download data: TXT
Series
Accession:
GSE28155
ID:
200028155
16.

Analysis of mRNA and EZH2 binding in TGF-B-treated A549 cells

(Submitter supplied) mRNA-seq of A549 cells carrying out EMT-MET in the absence or presence of the EZH2 inhibitor GSK126. In addition, we carried out ChIP-seq of EZH2 in A549 cells upon TGF-B treatment.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
14 Samples
Download data: BIGWIG
Series
Accession:
GSE180067
ID:
200180067
17.

Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

(Submitter supplied) Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFβ-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9250
13 Samples
Download data: BED
Series
Accession:
GSE45579
ID:
200045579
18.

Expression data from Sox4 knockdown cells in the presence and absence of TGFβ in NMuMG cells

(Submitter supplied) Expression profiling after Sox4 knockdown (KD) during epithelial to mesenchymal transition (EMT) in NMuMG reveals a significant number of genes that are transcriptionally deregulated.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE44050
ID:
200044050
19.

Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos

(Submitter supplied) Conditional ablation of Ezh2 in the neural crest lineage results in loss of the neural crest-derived mesenchymal derivatives. In this data sheet we determine gene expression analysis in Ezh2lox/lox and Wnt1Cre Ezh2lox/lox in E11.5 mouse BA1 cells.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE52220
ID:
200052220
20.

Lamin B1 loss promotes lung cancer development and metastasis by epigenetic derepression of RET

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18635 GPL19057
12 Samples
Download data: BW
Series
Accession:
GSE94681
ID:
200094681
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