Similar studies for GEO DataSets (Select 200081931) - GEO DataSets

Links from GEO DataSets

Items: 20

Select item 2000819311.

SNAI1 overexpression effect on MCF-10A mammary epithelial cell line

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

Organism:: synthetic construct; Homo sapiens

Type:: Expression profiling by array; Non-coding RNA profiling by array

Platforms:: GPL570 GPL14613
12 Samples

Download data: CEL

Series

Accession:: GSE81931

ID:: 200081931

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000819302.

SNAI1 overexpression effect on MCF-10A mammary epithelial cell line (miRNA)

(Submitter supplied) SNAI1 is a key transcription factor in the EMT process, that is considered as the initial step of metastasis. The microRNAs(miRNAs) invovled in SNAI1-induced EMT may play important roles in regulating the process of metastasis. We used microarrays to establish the miRNAs both upregulated and downregulated in SNAI1-induced EMT process.

Organism:: synthetic construct; Homo sapiens

Type:: Non-coding RNA profiling by array

Platform:: GPL14613
6 Samples

Download data: CEL

Series

Accession:: GSE81930

ID:: 200081930

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000819293.

SNAI1 overexpression effect on MCF-10A mammary epithelial cell line (mRNA)

(Submitter supplied) SNAI1 is a key transcription factor in the EMT process, that is considered as the initial step of metastasis. A lot of genes invovled in SNAI1-induced EMT may play important roles in regulating the process of metastasis. We used microarrays to establish the gene expression in SNAI1-induced EMT process.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL570
6 Samples

Download data: CEL

Series

Accession:: GSE81929

ID:: 200081929

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000585604.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000545055.

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

Series

Accession:: GSE54505

ID:: 200054505

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 2000384596.

miRNA profiles in head and neck natural epithelial - mesenchymal phenotype cell line pair, and in TGF-β induced EMT models

(Submitter supplied) Sixth generation Exiqon® locked nucleic acid miRCURY™ LNA microarrays were used to search and validate some unidentified miRNAs that regulate EMT in head and neck cancer carcinoma.

Organism:: Rattus norvegicus; Human alphaherpesvirus 2; Merkel cell polyomavirus; human gammaherpesvirus 4; JC polyomavirus; Human gammaherpesvirus 8; Mus musculus cytomegalovirus 2; Betapolyomavirus macacae; Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Murid betaherpesvirus 1; Human immunodeficiency virus 1; Homo sapiens; Murid gammaherpesvirus 4; Betapolyomavirus hominis

Type:: Non-coding RNA profiling by array

Platform:: GPL11434
3 Samples

Download data: TXT

Series

Accession:: GSE38459

ID:: 200038459

Select item 2000820587.

Transcriptomics response to miR-644 overexpression in three breast cancer cell lines

(Submitter supplied) The goal of the study is to investigate the effect of microRNA-644 overexpression by chemical mimics on gene expression in breast cancer cell lines. To this purpose control and microRNA-644 mimics are used to transfect MDA-MB-231 cells, SK-BR-3 cells, and MCF-7 cells respectively. Transcriptomics profiling was performed with Illumina HumanHT-12 V4.0 BeadChip microarray.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL10558
12 Samples

Download data: IDAT

Series

Accession:: GSE82058

ID:: 200082058

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000582528.

Expression data from breast cancer cell line MCF-7 with ectopic expression of the transcription factor Snail

(Submitter supplied) The transcription factor Snail has been proposed to mediate epithelial-to-mesenchymal transition (EMT) and confer mesenchymal invasive phenotype to epithelial cancer cells To analyze the molecular effects of ectopic Snail expression on an epithelial breast cancer cell line, gene expression profiles of MCF-7 cells transfected to overexpress Snail-6SA variant (MCF-7-Snail) and MCF-7 cells transfected with control plasmid (MCF-7-control) were compared. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL570
6 Samples

Download data: CEL, CHP

Series

Accession:: GSE58252

ID:: 200058252

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000622309.

Expression of miR-200c in claudin-low breast cancer alters stem cell functionality, enhances chemosensitivity and reduces metastatic potential

(Submitter supplied) Claudin-low tumors are a highly aggressive breast cancer subtype with no targeted treatments and a clinically documented resistance to chemotherapy. They are significantly enriched in cancer stem cells (CSCs), which makes claudin-low tumor models particularly attractive for studying CSC behavior and developing novel approaches to minimize CSC therapy resistance. One proposed mechanism by which CSCs arise is via an epithelial-mesenchymal transition (EMT), and reversal of this process may provide a potential therapeutic approach for increasing tumor chemosensitivity. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL11383
7 Samples

Download data

Series

Accession:: GSE62230

ID:: 200062230

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20020665810.

MLL3 Loss Drives Metastasis by Promoting a Hybrid Epithelial-Mesenchymal Transition State [ATAC-seq]

(Submitter supplied) Phenotypic plasticity associated with the hybrid epithelial-mesenchymal transition (EMT) state is crucial to metastatic seeding and outgrowth. We showed that deletion of the epigenetic regulator MLL3, a tumor suppressor frequently altered in human cancer, promoted the acquisition of the hybrid EMT state in both epithelial and mesenchymal breast cancer cells by facilitating EMT and MET, distinct from other known EMT regulators mediating unidirectional changes. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL24676
8 Samples

Download data: BW

Series

Accession:: GSE206658

ID:: 200206658

PubMed Full text in PMC Similar studies

Select item 20020665711.

MLL3 Loss Drives Metastasis by Promoting a Hybrid Epithelial-Mesenchymal Transition State [ChIP-seq UTX and MLL4]

(Submitter supplied) Phenotypic plasticity associated with the hybrid epithelial-mesenchymal transition (EMT) state is crucial to metastatic seeding and outgrowth. However, the mechanisms controlling the induction of hybrid EMT remain poorly defined. We showed that deletion of the epigenetic regulator MLL3, a tumor suppressor frequently altered in human cancer, promoted the acquisition of the hybrid EMT state in both epithelial and mesenchymal breast cancer cells by facilitating EMT and MET, distinct from other known EMT regulators mediating unidirectional changes. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL24676
12 Samples

Download data: BW

Series

Accession:: GSE206657

ID:: 200206657

PubMed Full text in PMC Similar studies

Select item 20020665612.

MLL3 Loss Drives Metastasis by Promoting a Hybrid Epithelial-Mesenchymal Transition State [ChIP-seq histone marker]

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL20301
16 Samples

Download data: BW

Series

Accession:: GSE206656

ID:: 200206656

PubMed Full text in PMC Similar studies

Select item 20020665513.

MLL3 Loss Drives Metastasis by Promoting a Hybrid Epithelial-Mesenchymal Transition State [RNA-seq MDA231 KO vs WT]

(Submitter supplied) Loss of MLL3 facilitates mesenchymal cells to acquire a mesenchymal/epithelial hybrid state during metastatic colonization. MLL3 loss led to IFNg signaling upregulation, which contributes to the induction of hybrid EMT cells and the enhanced metastatic capacity. Here we reported the gene expression profiles of WT and MLL3-KO MDA-MB-231 cells.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
6 Samples

Download data: CSV

Series

Accession:: GSE206655

ID:: 200206655

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20020665314.

MLL3 Loss Drives Metastasis by Promoting a Hybrid Epithelial-Mesenchymal Transition State [RNA-seq EM vs M]

(Submitter supplied) Loss of MLL3 facilitates mesenchymal cells to acquire a mesenchymal/epithelial hybrid state during metastatic colonization. The MET occurring in distant metastases is likely driven by stromal signals in the metastatic niche. One signaling pathway that promotes the MET is the activation of protein kinase A (PKA). The MET hybrid cells can be identified as CD44+CD104+/high. Forskolin treatment generated significantly more CD44+CD104high hybrid cells in MLL3-mutant cells than the WT MDA-MB-231 cells. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
6 Samples

Download data: CSV

Series

Accession:: GSE206653

ID:: 200206653

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20017144715.

MLL3 loss drives metastasis and therapeutic resistance by promoting a hybrid EMT state

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

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing; Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL20301 GPL16686 GPL24676
54 Samples

Download data: BW, CEL, CHP

Series

Accession:: GSE171447

ID:: 200171447

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20017144516.

Effect of Mll3 deletion in MCF7 cells

(Submitter supplied) MLL3 inactivation mutations occurs frequently in human breast cancer. To understand the function of MLL3 inactivation, we compared the gene expression profiles of the vector control (WT) and Mll3-knockout MCF7 cells generated by CRISPR-CAS9. Affymetrix human Gene 2.0ST arrays were used for microarray.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL16686
6 Samples

Download data: CEL, CHP

Series

Accession:: GSE171445

ID:: 200171445

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20017144417.

MLL3 loss drives metastasis and therapeutic resistance by promoting a hybrid EMT state [RNA-seq]

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
6 Samples

Download data: CSV

Series

Accession:: GSE171444

ID:: 200171444

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20001963118.

Global changes in gene expression in response to miR-200 overexpression in 4TO7 cells

(Submitter supplied) Transcriptional profiling of 4TO7 cells stably overexpressing miR-200s or CDH1. We observe a dramatic shift in the gene signatures when miR-200s (cluster 2; miR-200c/141, or both clusters) are overexpressed relative to controls. However, cluster 1 overexpression (miRs-200b/a/429) alone or CDH1 overexpression does not induce global changes in gene expression to levels observed for cluster 2 (miR-200c/141) or both clusters together.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL4134
16 Samples

Download data: TXT

Series

Accession:: GSE19631

ID:: 200019631

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20001574119.

Gene expression profiles of forced miR-200 expression in 344SQ lung adenocarcinoma cells with high metastatic potential

(Submitter supplied) Metastatic disease is a primary cause of cancer-related death, and factors governing tumor cell metastasis have not been fully elucidated. Here we addressed this question by using tumor cell lines derived from mice that develop metastatic lung adenocarcinoma owing to expression of mutant K-ras and p53. A feature of metastasis-prone tumor cells that distinguished them from metastasis-incompetent tumor cells was plasticity in response to changes in their microenvironment. more...