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Links from GEO DataSets

Items: 20

1.

The dual role of Irf1 in maintaining epithelial identity while enabling EMT

(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:
GPL19057 GPL17021
16 Samples
Download data: BIGWIG
Series
Accession:
GSE141502
ID:
200141502
2.

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

(Submitter supplied) To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we performed chromatin immunoprecipitation with Irf1-specific antibodies in NMuMG cells treated for 2 days with TGFbeta or left untreated (0d TGFbeta). Intersection with RNA-sequencing after downregulation of Irf1 with or without treatment with TGFbeta for two days revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: BIGWIG
Series
Accession:
GSE141501
ID:
200141501
3.

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

(Submitter supplied) To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we downregulated Irf1 by siRNA and analyzed differentially regulated genes and pathways upon EMT induction (2 days TGFbeta) or in the absence of EMT (0 day TGFbeta). Intersection with Irf1 ChIP-sequencing after 2 days of TGFbeta treatment or in untreated cells revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: TXT
Series
Accession:
GSE141500
ID:
200141500
4.

Foxf2 plays a dual role during TGFb-induced EMT by promoting apoptosis yet enabling cell junction dissolution and migration.

(Submitter supplied) We have identified the transcription factor forkhead box protein F2 (Foxf2) to be upregulated in its expression during the EMT process and studied its functional contribution to EMT by siRNA-mediated knockdown in NMuMG cells treated for 4 days with TGFbeta followed by mRNA-sequencing. Our analysis revealed a dual role of Foxf2 during TGFbeta-induced EMT in promoting apoptosis while inducing cell junction breakdown and migration.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE112796
ID:
200112796
5.

Elf5 inhibits epithelial mesenchymal transition in development and cancer metastasis through transcriptional repression of Snail2

(Submitter supplied) Elf5 (or ESE-2) is an ETS transcription factor that is abundantly expressed in the mammary epithelium, where it plays a critical role in dictating cell fate and lineage choices. These changes are in part mediated by alterations in the expression and activity of critical components of the Jak/Stat pathway. While the biological function of Elf5 in mammary gland development has been well characterized, its role in breast cancer remains to be elucidated. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
10 Samples
Download data: TXT
Series
Accession:
GSE32150
ID:
200032150
6.

MDA-MB-231 cell: infected with lentivirus to stably express mut-Elf5 vs WT-Elf5

(Submitter supplied) Elf5 induced transcriptional changes in MDA-MB-231 origin, control (mut Elf5) vs WT ELF5
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
6 Samples
Download data: TXT
Series
Accession:
GSE32144
ID:
200032144
7.

LM2 cell: infected with lentivirus to stably express Elf5 vs GFP

(Submitter supplied) Elf5 induced transcriptional changes in high lung metastasis subline LM2 (MDA-MB-231 origin), control (GFP) vs ELF5
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
4 Samples
Download data: TXT
Series
Accession:
GSE32143
ID:
200032143
8.

Expression data from mice mammary glands from Elf5 knockout (KO) and wildtype controls

(Submitter supplied) We developed conditional knockout mice where the transcription factor Elf5 (also called ESE-2) is deleted in the mammary glands. Loss of Elf5 results in block in alveologenesis and epithelial differentiation defects. Mammary gland samples from Elf5 knockout and wild type animals were analyzed for global transcriptome changes.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE32103
ID:
200032103
9.

Tead2 expression levels control the subcellular distribution of Yap and Taz, zyxin expression and epithelial-mesenchymal transition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL13112 GPL6246
8 Samples
Download data: CEL, WIG
Series
Accession:
GSE55711
ID:
200055711
10.

Tead2 expression levels control the subcellular distribution of Yap and Taz, zyxin expression and epithelial-mesenchymal transition (expression)

(Submitter supplied) Cellular changes during an epithelial-mesenchymal transition (EMT) largely rely on global changes in gene expression orchestrated by transcription factors. Tead transcription factors and their co-factors Yap and Taz have been shown to be implicated in EMT, nevertheless, their direct and indirect target genes during EMT have remained elusive. We used microarrays to detail the changes in global programme of gene expression during TGFβ-induced EMT in a murine breast cancer cell line (Py2T).
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
4 Samples
Download data: CEL
Series
Accession:
GSE55710
ID:
200055710
11.

Tead2 expression levels control the subcellular distribution of Yap and Taz, zyxin expression and epithelial-mesenchymal transition (ChIP-seq)

(Submitter supplied) Cellular changes during an epithelial-mesenchymal transition (EMT) largely rely on global changes in gene expression orchestrated by transcription factors. Tead transcription factors and their co-factors Yap and Taz have been shown to be implicated in EMT, nevertheless, their direct target genes during EMT have remained elusive.We used genome-wide chromatin immunoprecipitation and next generation sequencing to identify diect Tead2 target genes during EMT.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: WIG
Series
Accession:
GSE55709
ID:
200055709
12.

E-cadherin re-expression shows in vivo evidence for mesenchymal to epithelial transition in clonal metastatic breast tumor cells

(Submitter supplied) Substantial experimental evidence has shown that dedifferentiation from an epithelial state to a mesenchymal-like state (EMT) drives tumor cell metastasis. This transition facilitates tumor cells to acquire motility and invasive features. Intriguingly, tumor cells at the metastatic site are primarily epithelial, and it is believed that they re-differentiate back to an epithelial state by a process called mesenchymal to epithelial transition (MET). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
4 Samples
Download data: CEL
Series
Accession:
GSE81033
ID:
200081033
13.

A critical role of histone deacetylases, Mbd3/NuRD and Tet2 in epithelial-mesenchymal cell plasticity and in tumor invasion and metastasis

(Submitter supplied) We have generated and employed reversible and irreversible EMT models of murine breast cancer cells to identify the key players establishing cell state transitions during a reversible and an irreversible EMT. We demonstrate that the Mbd3/NuRD complex, involving histone deacetylases (HDACs) and Tet2 hydroxylase, acts as an epigenetic block in epithelial-mesenchymal plasticity. These epigenetic modifiers keep breast cancer cells in a stable mesenchymal state, and their pharmacological inhibition or genetic ablation leads to a mesenchymal-epithelial transition (MET) and represses primary tumor growth and metastasis formation of highly aggressive, mesenchymal breast cancer cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL19057
20 Samples
Download data: TXT
Series
Accession:
GSE100553
ID:
200100553
14.

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
15.

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
16.

Rb deletion in mammary stem/progenitor epithelium induces tumors with features of luminal-B or basal-like breast cancer

(Submitter supplied) The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL4092 GPL891 GPL2881
144 Samples
Download data
Series
Accession:
GSE14457
ID:
200014457
17.

A kinome-wide high-content siRNA screen identifies MEK5-ERK5 signaling as critical for breast cancer cell EMT and metastasis

(Submitter supplied) We have employed a high-content microscopy screen in combination with a kinome and phosphatome-wide siRNA library to identify signaling pathways underlying an EMT of murine mammary epithelial cells and breast cancer cells. This screen identified the MEK5-ERK5 axis as a critical player in TGFb-mediated EMT. Suppression of MEK5-ERK5 signaling completely prevented the morphological and molecular changes occurring during a TGFb-induced EMT and, conversely, forced highly metastatic breast cancer cells into a differentiated epithelial state. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: TXT
Series
Accession:
GSE100403
ID:
200100403
18.

Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition

(Submitter supplied) The Runx1 transcription factor is essential for hematopoietic differentiation and mutations underlie various leukemias. Here we demonstrate a role for Runx1 in the MCF10 cell series model of breast cancer progression. The highest level of Runx1 that occurs in normal like mammary epithelial cells (MCF10A) is decreased in tumorigenic (MCF10AT1) and metastatic (MCF10CA1a) breast cancer cells. We show that depletion of Runx1 in MCF10A cells results in striking changes in cell morphology and induction of epithelial-mesenchymal transition (EMT) via several signaling pathways. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
6 Samples
Download data: TXT
19.

LincK promotes proliferation and epithelial-to-mesenchymal transition and contributes to tumorigenesis and growth in breast cancer II

(Submitter supplied) We previously reported that transwell co-culture with hAD-MSCs cells can induce an EMT progress in MCF7 cells. To identify EMT-relevant lncRNAs, we conducted transcriptome microarray analysis of MCF7 cells at Day 0, 2, 4, 6, 8 and 10 after coculture.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL19072
6 Samples
Download data: TXT
Series
Accession:
GSE109008
ID:
200109008
20.

LincK promotes proliferation and epithelial-to-mesenchymal transition and contributes to tumorigenesis and growth in breast cancer I

(Submitter supplied) In this study, we aimed to identify potential lncRNA deregulations associated with breast cancer malignancy instigated by MSCs-MCF7 co-culture. We profiled expression changes of lncRNAs in MCF-7 cells during EMT induced by coculture with hAD-MSCs, and found an intergenic lncRNA with proviouly unknown function (KB-1732A1.1, we termed it LincK), which was significantly elevated. Depletion of LincK decreased the growth, migration, invasion, and EMT in breast cancer cells, while overexpression of LincK exerted the opposite effects. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
9 Samples
Download data: CEL
Series
Accession:
GSE109007
ID:
200109007
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