Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells.

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE35911: Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells [Expression] GSE35912: Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells [Methylation] Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Jason Lai

PROVIDER: E-GEOD-35913 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Reversal of aberrant cancer methylome and transcriptome upon direct reprogramming of lung cancer cells.

Mahalingam Dashayini D Kong Chiou Mee CM Lai Jason J Tay Ling Lee LL Yang Henry H Wang Xueying X

Scientific reports 20120821

Recent reports on direct reprogramming of cancer cells (iPCs) which results in reduced tumorigenic potential has attributed the importance of epigenetics in tumorigenesis, but lacked genome-wide analysis. Here we describe successful generation of iPCs from non-small cell lung cancer (NSCLC) cell lines. Following reprogramming, they resembled embryonic stem and induced pluripotent stem cells in pluripotency markers expression, gene expression patterns and in vitro differentiation ability. Genome- ...[more]

PMID: 22912920

Similar Datasets

Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells [Expression]

Project description:Non-small cell lung cancer cell (NSCLC) lines were reprogrammed with Yamanaka's cocktail and their methylome and transcriptome were studied and characterized. We compared reprogrammed cells to their respective parent (2 NSCLC and 1 human lung fetal fibroblast) and used H1 as a positive control for pluripotency characteristics. The in vitro differentiated cells were also compared to the reprogrammed cells. All samples have biological triplicates except for differentiated cells.

2012-09-01 | E-GEOD-35911 | biostudies-arrayexpress

Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells [Methylation]

2012-09-01 | E-GEOD-35912 | biostudies-arrayexpress

Gene expression profiling of human colon cancer cell lines stimulated with dsDNA90

Project description:Gene expression analysis of dsDNA90 stimulated human colon cancer cell lines. Genes whose expression that are affected by cytosolic DNA will be identified and compared between normal vs cancer colon epithelial cells. Human normal or colon cancer cells were transfected with dsDNA90 for 3 hours. Total RNA was extracted for array analysis.

2015-11-21 | E-GEOD-75205 | biostudies-arrayexpress

Project description:Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells.

| PRJNA152011 | ENA

A profibrotic gene expression program induced by Egr-1 in skin fibroblasts

Project description:Systemic sclerosis (SSc) is characterized by vascular damage, autoimmunity and fibrosis and is associated with highly variable clinical presentation and disease course. Aberrant transforming growth factor-ß (TGF-ß) signaling via the early immediate transcription factor Egr-1 is implicated in the pathogenesis of SSc. To shed light on the role of Egr-1 in fibrosis, regulation of gene expression in human skin fibroblasts overexpressing Egr-1 was examined by genome-wide expression analysis. Over 600 genes were found to be regulated by Egr-1. The Egr-1-responsive gene signature is largely comprised of genes involved in cell proliferation, TGF-ß signaling, wound healing, extracellular matrix synthesis and vascular development. Expression of the Egr-1 responsive genes was evaluated in a microarray dataset comprising skin biopsies from 17 patients with scleroderma and six healthy controls (GEO GSE9285; PMID 18648520). The “Egr-1 responsive gene signature” was enriched in the ‘diffuse-proliferation’ subset of skin biopsies in the patients with diffuse cutaneous SSc (dcSSc), but was not associated with other forms of scleroderma, or with healthy controls. Skin biopsies from patients with scleroderma can provide more insights into the relevant pathological processes in the subset of disease and could be developed into a diagnostic tool for identifying a subset of diffuse scleroderma patients who may be responsive to Egr-1 therapy. Cultures of primary fibroblasts from neonatal foreskin treated by Egr1 and Tgfb1 were measured at 24 and 48 hours. Control samples without any treatment were also measured at the same time points. Two biological replicates per condition/time point were measured using the Illumina HumanRef-8 V2 Expression BeadChip.

2011-10-25 | E-GEOD-27165 | biostudies-arrayexpress

Homo sapiens

Project description:Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells [Expression]

| PRJNA155695 | ENA

Homo sapiens

Project description:Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells [Methylation]

| PRJNA155697 | ENA

Combinatorial treatment of DNMT inhibitor and LSD1 inhibitor results in cell growth inhibition and reexpression of epigenetically silenced genes (gene expression)

Project description:A combinatorial treatment consisting of a DNMTi and a LSD1i shows synergistic effects in reactivating aberrantly silenced genes by enriching H3K4me2 and H3K4me. 24 Samples consisting of 3 cell lines hybridised to the Illumina HumanHT-12 V4.0 Beadchip.

2013-08-01 | E-GEOD-41676 | biostudies-arrayexpress

Inhibition of Melanoma Growth by Small Molecules that Promote the Mitochondrial Localization of ATF2

Project description:Effective therapy for malignant melanoma, the leading cause of death from skin cancer, remains an area of significant unmet need in oncology. Increased expression of PKC? in advanced metastatic melanoma, results in the phosphorylation of the transcription factor ATF2 on threonine 52, which causes its nuclear localization and confers its oncogenic activities. The nuclear-to-mitochondrial translocation of ATF2 following genotoxic stress promotes apoptosis, a function that is largely lost in melanoma cells, due to its confined nuclear localization. Therefore, promoting the nuclear export of ATF2, which sensitizes melanoma cells to apoptosis, offers a novel therapeutic modality. We conducted a pilot high-throughput screen of 3,800 compounds to identify small molecules that promote melanoma cell death by inducing the cytoplasmic localization of ATF2. For this specific gene expression analysis experiment, we subjected WM793 melanoma cells to treatment with DMSO- or 10µM SBI-0087702 for 24 h. RNA was harvested and subjected to microarray analyses using the Illumina Human HT-12 v4 BeadChip. Raw microarray data were normalized using the lumi package in R (variant stabilizing transformation followed by quantile normalization). Subsequent variant-stabilized, normalized microarray values were sorted by fold-change values and subjected to a 1.5-fold-change cut-off threshold. The fold-change-ranked gene list was subjected to gene ontological enriched functional network clustering using the Ingenuity (IPA) gene ontology platform.

2012-12-28 | E-GEOD-43135 | biostudies-arrayexpress

Type 2 innate signals regulate functionality of fibro/adipogenic progenitors to facilitate muscle regeneration

Project description:In vertebrates, activation of innate immunity is an early response to injury, implicating it in the regenerative process. However, the mechanisms by which innate signals might regulate stem cell functionality are unknown. Here we demonstrate that type 2 innate immunity is required for regeneration of skeletal muscle after injury. Muscle damage results in rapid recruitment of eosinophils, which secrete IL-4 to activate the regenerative actions of muscle resident fibro/adipocyte progenitors (FAPs). In FAPs, IL-4/IL-13 signaling serves as a key switch to control their fate and functions. Activation of IL-4/IL-13 signaling promotes proliferation of FAPs to support myogenesis, while inhibiting their differentiation into adipocytes. Surprisingly, type 2 cytokine signaling is also required in FAPs, but not myeloid cells, for rapid clearance of necrotic debris, a process that is necessary for timely and complete regeneration of tissues. Fibroadipocyte progenitors were isolated from wild-type and IL-4Ra knockout (IL-4Ra -/-) mice and were treated with vehicle or IL4 stimulation in culture prior to microarray analysis. 4 biological replicates of each condition were performed.

2013-04-11 | E-GEOD-44933 | biostudies-arrayexpress

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