GEO DataSets

(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

(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:

Homo sapiens; synthetic construct

Type:

Non-coding RNA profiling by array

Platform:

GPL14613

6 Samples

Download data: CEL

(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

(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

(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

(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:

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; Rattus norvegicus; Human alphaherpesvirus 2; Merkel cell polyomavirus

Type:

Non-coding RNA profiling by array

Platform:

GPL11434

3 Samples

Download data: TXT

(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

(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

(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

(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

(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

(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:

GPL20301

16 Samples

Download data: BW

(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

(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

(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

(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

(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

(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

(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...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

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

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL339 GPL1261

28 Samples

Download data: CEL