GEO DataSets

(Submitter supplied) Tumors that show evidence of epithelial to mesenchymal transition (EMT) have been associated with metastasis, drug resistance, and poor prognosis. EMT may alter the molecular requirements for growth and survival in different contexts, but the underlying mechanisms remain incomplete. Given the heterogeneity along the EMT spectrum between and within tumors it is important to define the requirements for growth and survival in cells with an epithelial or mesenchymal phenotype to maximize therapeutic efficacy. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

6 Samples

Download data: CEL, CHP

(Submitter supplied) To determine the difference of gene expression profile in epithelial and mesenchymal KRAS mutant lung cancers, epithelial NCI-H358 cells were treated with TGFβ1 (4 ng/mL) or PBS for 14 days in order to induce epithelial to mesenchymal transition (EMT). Gene expression was determined in NCI-H358 cells before and after EMT induction. In addition, in order to investigate the effect of a MEK inhibitor trametinib on gene expression, mesenchymal NCI-H1792 cells were treated with 50 nM trametinib for 48 hours. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17077

8 Samples

Download data: TXT

(Submitter supplied) Mutations in PIK3CA, the gene encoding the p110α subunit of PI3K, induce transformation of mammary epithelial cells (MEC). Studies suggest the transforming action of mutant PIK3CA requires binding to activated receptor tyrosine kinases or adaptors. We examined in transgenic mice if ErbB3, a powerful activator of PI3K, is required for mutant PIK3CA-mediated MEC transformation. ErbB3 loss delayed PIK3CAH1047R-dependent mammary gland hyperplasia, but tumor latency, gene expression and markers of PI3K signaling were unaffected. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11383

12 Samples

Download data

(Submitter supplied) A variety of mechanotransduction forces are altered in the tumor microenvironment (TME) and these biophysical forces can influence cancer progression. One such force is interstitial fluid flow (IFF) - the movement of fluid through the tissue matrix. IFF was previously shown to induce invasion of cancer cells, but the activated signaling cascades remain poorly understood. Here, it is demonstrated that IFF induces invasion of ERBB2/HER2 expressing breast cancer cells via activation of phosphoinositide-3-kinase (PI3K). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5800

Platform:

GPL10558

12 Samples

Download data: TXT

Analysis of non-invasive NeuN cells and invasive NeuT cells (i.e., MCF10A cells overexpressing wild-type ERBB2 or a constitutively active mutant of ERBB2, respectively) treated with IFF. Results provide insight into the molecular pathways activated by IFF in ERBB2-positive breast cancer cells.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 cell line, 2 protocol sets

Platform:

GPL10558

Series:

GSE64670

12 Samples

Download data

(Submitter supplied) ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

18 Samples

Download data: CSV, TAB

(Submitter supplied) ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: BROADPEAK, TXT

(Submitter supplied) ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

6 Samples

Download data: CSV, TAB

(Submitter supplied) ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

3 Samples

Download data: BROADPEAK

(Submitter supplied) ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

4 Samples

Download data: BROADPEAK, TXT

(Submitter supplied) ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

12 Samples

Download data: CSV, TAB

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus; Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL18573 GPL19057

51 Samples

Download data: BROADPEAK, TAB

(Submitter supplied) Mammary organoids harvested from ErbB3 DOX-KO mice, which utilize MMTV-Cre transgene expression in the LE to cause genomic recombination at floxed ErbB3 alleles in ErbB3FL/FL were cultured in the presence or absence of doxycycline to induce ErbB3 loss. The gene expression shift following DOX-induced ErbB3 loss in the 3D organoids was examined by microarray.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

6 Samples

Download data: CEL

(Submitter supplied) The PTEN/PI3K pathway is commonly mutated in cancer and therefore represents a rational target for therapeutic intervention. In order to investigate the primary phenotype(s) mediated by mutant PIK3CA in a clean and highly patient-relevant context, we utilized a non-tumorigenic MCF10A parental and isogenic knock-in cell line that harbors a common activating PIK3CA kinase domain mutation (H1047R). We found that introduction of an endogenously mutated PIK3CA primarily results in a marked epithelial-mesenchymal transition (EMT) and invasive phenotype compared to isogenic wild-type cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

12 Samples

Download data: CEL

(Submitter supplied) RNA sequencing analysis of A549 cells that were depleted for ARAF (shARAF) and reconstituted with either empty vector control (+EV) or ARAF wildtype (+ARAF) or dimer deficient ARAF kinase (+R362H) respectively to identify factors that are differentially regulated by ARAF and its kinase activity. In particular, we discovered that ARAF regulates genes that are involved in proliferation and malignant growth by surpressing gene expression of members of the ERBB3/ AKT signaling pathway. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: TSV

(Submitter supplied) We investigated the role of PME-1 (protein phosphatase methylesterase-1) as a specific methylesterase for the critical cancer suppressor, protein phosphatase 2A (PP2A), and its potential contributions to the development and malignancy of various cancers. Notably, no gene expression database related to PME-1 deficiency had been previously reported. To address this knowledge gap, we conducted an analysis of the impact of PME-1 on gene expression using mouse embryonic fibroblasts (MEFs) isolated from both PME-1 wild-type (WT) and knockout (KO) mice.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

6 Samples

Download data: TXT

(Submitter supplied) Recent findings show that EMT in cancer is dynamic and display a number of intermediate stages along the transition to obtain a high phenotypic and functional cellular plasticity. To comprehend transcriptional regulation among major EMT-transcription factors (EMT-TFs) along the EMT spectrum, we performed gene expression profiles of EMT-TFs (SNAI1/2, ZEB1/2, TWIST1) overexpressing epithelial (PEO1, OVCA420) and intermediate epithelial (OVCA429) ovarian cancer cell clones. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17586

28 Samples

Download data: CEL