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Links from GEO DataSets

Items: 20

1.

Twist1 and Slug mediate H2A.X-regulated epithelial-mesenchymal transition in breast cells

(Submitter supplied) The epithelial-mesenchymal transition (EMT) is thought to be essential for cancer metastasis. While chromatin remodeling is involved in EMT, histone variants contribution in EMT remains poorly investigated. Recently, we showed that silencing or removal of the histone variant H2A.X induced mesenchymal-like characteristics, including activation of the EMT transcription factors, Slug and ZEB1, in human colon cancer cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
10 Samples
Download data: CEL
Series
Accession:
GSE80180
ID:
200080180
2.

The histone variant H2A.X is a regulator of Epithelial–Mesenchymal Transition

(Submitter supplied) The epithelial-mesenchymal transition (EMT), considered essential for metastatic cancer, has been a focus of much research, but important questions remain. Here, we show that silencing or removing H2A.X, a histone H2A variant involved in cellular DNA repair and robust growth, induced mesenchymal-like characteristics including activation of EMT transcription factors, Slug and ZEB1, in HCT116 human colon cancer cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
9 Samples
Download data: CEL
Series
Accession:
GSE75444
ID:
200075444
3.

Transcriptional changes associated with overexpression of TBX3 isoforms (TBX3iso1 and TBX3iso2) in the DCIS-like 21NT cell line

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL5082
18 Samples
Download data: CEL
Series
Accession:
GSE126156
ID:
200126156
4.

Transcriptional changes associated with overexpression of TBX3 isoforms (TBX3iso1 and TBX3iso2) in the DCIS-like 21NT cell line (ChIP)

(Submitter supplied) Purpose: The acquisition of cellular invasiveness of breast epithelial cells and subsequent transition from ductal carcinoma in situ (DCIS) to invasive breast cancer is a critical step in breast cancer progression. Very little is known about the molecular dynamics governing this transition. We have previously shown that overexpression of the transcriptional regulator TBX3 in DCIS-like 21NT cells results in increased survival, growth, and invasiveness. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by array
Platform:
GPL5082
12 Samples
Download data: CEL, TXT, XLS
Series
Accession:
GSE126154
ID:
200126154
5.

Transcriptional changes associated with overexpression of TBX3 isoforms (TBX3iso1 and TBX3iso2) in the DCIS-like 21NT cell line (RNA-Seq)

(Submitter supplied) Purpose: The acquisition of cellular invasiveness of breast epithelial cells and subsequent transition from ductal carcinoma in situ (DCIS) to invasive breast cancer is a critical step in breast cancer progression. Very little is known about the molecular dynamics governing this transition. We have previously shown that overexpression of the transcriptional regulator TBX3 in DCIS-like 21NT cells results in increased survival, growth, and invasiveness. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TXT, XLSX
6.

Loss of BRMS1 promotes a mesenchymal phenotype through regulation of Twist1

(Submitter supplied) Analysis of BRMS1 KD-induced EMT in non-samll cell lung cancer at gene expression level. The hypothesis tested in the present study was that BRMS1 KD induces EMT through differential regulation of EMT genes and Twist1 KD restores the epithelial phenotype in cells with BRMS1 KD. Results provide important information of biological functions in lung cancer which BRMS1 KD involves in, such as EMT, signaling, biological adhesion, immune system process, response to stimulus, and so on.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
6 Samples
Download data: TXT
Series
Accession:
GSE62359
ID:
200062359
7.

TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis

(Submitter supplied) Using a TWIST1-inducible epithelial-to-mesenchymal transition (EMT) model in HMLE cells, miRNA changes were profiled at different time points during an active EMT.
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL18795
12 Samples
Download data: TXT
Series
Accession:
GSE58560
ID:
200058560
8.

TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis

(Submitter supplied) Epithelial-to-mesenchymal transition (EMT) is a dynamic process that relies on cellular plasticity; an EMT/MET axis is critical for metastatic colonization of carcinomas. Unlike epithelial programming, regulation of mesenchymal programming is not well understood in EMT. Here we describe the first microRNA that enhances exclusively mesenchymal programming. We demonstrate that microRNA-424 is up-regulated early during a TWIST1/SNAI1-induced EMT, and that it causes cells to express mesenchymal genes without affecting epithelial genes, resulting in a mixed/intermediate EMT. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
9.

Expression data from genetically modified HMLE human mammary epithelial cells

(Submitter supplied) Microarrays were used to determine relative global gene expression changes upon introduction of EMT-inducing or control vectors.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3921
21 Samples
Download data: CEL
Series
Accession:
GSE24202
ID:
200024202
10.

Analysis of the effects of loss of E-cadherin and cell adhesion on human mammary epithelial cells

(Submitter supplied) Loss of the epithelial adhesion molecule E-cadherin is thought to enable metastasis by disrupting intercellular contacts - an early step in metastatic dissemination. To further investigate the molecular basis of this notion, we use two methods to inhibit E-cadherin function that distinguish between E-cadherin's cell-cell adhesion and intracellular signaling functions. While the disruption of cell-cell contacts alone does not enable metastasis, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition, invasiveness and anoikis-resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3921
12 Samples
Download data: CEL
Series
Accession:
GSE9691
ID:
200009691
11.

Twist expression in HMLE and breast cancer T47D cells

(Submitter supplied) Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
8 Samples
Download data: CEL, CHP
Series
Accession:
GSE53222
ID:
200053222
12.

Dependency of NELF-E-SLUG-KAT2B epigenetic axis in breast cancer carcinogenesis

(Submitter supplied) Cancer cells undergo transcriptional reprogramming to drive tumorigenesis and caner progression. Here, we identified the transcriptional complex, NELF (Negative elongation factor), as an important regulator of this process. Using cancer cell lines and patient-derived tumor organoids, we demonstrated that loss of NELF inhibits breast cancer. Specifically, we found that epithelial-mesenchymal transition (EMT) and stemness-associated genes are downregulated in NELF-depleted breast cancer cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL20301
76 Samples
Download data: BED, BW, RESULTS, XLSX
Series
Accession:
GSE195761
ID:
200195761
13.

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL9115 GPL9442
19 Samples
Download data: TXT
Series
Accession:
GSE53026
ID:
200053026
14.

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition [DREAM-seq]

(Submitter supplied) Purpose: to characterize epigenetic changes following Twist1 mediated Epithelial-Mesenchymal Transition in human Methods: we characterized the epigenetic and transcriptome landscapes using whole genome transcriptome analysis by RNA-seq, DNA methylation by digital restriction enzyme analysis of methylation (DREAM) and histone modifications by CHIP-seq of H3K4me3 and H3K27me3 in immortalized human mammary epithelial cells relative to cells induced to undergo EMT by Twist1. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL9115
4 Samples
Download data: TXT
Series
Accession:
GSE53025
ID:
200053025
15.

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition [RNA-seq]

(Submitter supplied) Purpose: to characterize epigenetic changes following Twist1 mediated Epithelial-Mesenchymal Transition in human Methods: we characterized the epigenetic and transcriptome landscapes using whole genome transcriptome analysis by RNA-seq, DNA methylation by digital restriction enzyme analysis of methylation (DREAM) and histone modifications by CHIP-seq of H3K4me3 and H3K27me3 in immortalized human mammary epithelial cells relative to cells induced to undergo EMT by Twist1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9442
3 Samples
Download data: TXT
Series
Accession:
GSE53024
ID:
200053024
16.

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition [ChIP-seq]

(Submitter supplied) Purpose: to characterize epigenetic changes following Twist1 mediated Epithelial-Mesenchymal Transition in human Methods: we characterized the epigenetic and transcriptome landscapes using whole genome transcriptome analysis by RNA-seq, DNA methylation by digital restriction enzyme analysis of methylation (DREAM) and histone modifications by CHIP-seq of H3K4me3 and H3K27me3 in immortalized human mammary epithelial cells relative to cells induced to undergo EMT by Twist1. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
12 Samples
Download data: TXT
Series
Accession:
GSE53023
ID:
200053023
17.

SWI/SNF Chromatin-Remodeling Factor Smarcd3/Baf60c Controls Epithelial-Mesenchymal Transition by Inducing Wnt5a Signaling

(Submitter supplied) We previously identified a gene signature predicted to regulate the epithelial-mesenchymal transition (EMT) in both epithelial tissue stem cells and breast cancer cells. A phenotypic RNA interference (RNAi) screen identified the genes within this 140-gene signature that promoted the conversion of mesenchymal epithelial cell adhesion molecule-negative (EpCAM-) breast cancer cells to an epithelial EpCAM+/high phenotype. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL7504
18 Samples
Download data
Series
Accession:
GSE40145
ID:
200040145
18.

The expression level of microRNA after knockdown of Twist1 or Bmi1

(Submitter supplied) To screen the microRNA regulated by Twist1 and Bmi1
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL10656
3 Samples
Download data: TXT
Series
Accession:
GSE29586
ID:
200029586
19.

Transcriptome analysis of OECM1 after expression of let-7i

(Submitter supplied) Expression of let-7i results in transcriptome alteractions in head and neck cancer cell line, OECM1.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
2 Samples
Download data: CEL, CHP
Series
Accession:
GSE29539
ID:
200029539
20.

Next Generation Sequencing Facilitates Quantitative Analysis of SETD6 Knock-out and stable expression of TWIST1 in Glioblastoma cells

(Submitter supplied) The goal of this study was to identifiy shared target genes for SETD6 and TWIST1 in Glioblastoma.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
13 Samples
Download data: TSV, TXT
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