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Links from GEO DataSets

Items: 20

1.

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:
GPL24676 GPL20301 GPL16686
54 Samples
Download data: BW, CEL, CHP
Series
Accession:
GSE171447
ID:
200171447
2.

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
3.

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
4.

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

(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
Series
Accession:
GSE206656
ID:
200206656
5.

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
6.

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
7.

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
8.

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

(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
9.

A complex epigenome-splicing crosstalk governs epithelial to mesenchymal transition in metastasis and brain development

(Submitter supplied) Epithelial to Mesenchymal Transition (EMT) renders epithelial cells migratory properties. While epigenetic and splicing changes have been implicated in EMT, the mechanisms governing their crosstalk remain poorly understood. Here, we discovered a C2H2 zinc finger protein, ZNF827, is strongly induced during various contexts of EMT including in brain development and breast cancer metastasis and is required for the molecular and phenotypic changes underlying EMT in these processes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL11154
24 Samples
Download data: BED, BW, TXT
Series
Accession:
GSE173874
ID:
200173874
10.

Single cell RNA sequencing on PyMT mammary gland primary tumor and lung metastases

(Submitter supplied) Using scRNA-seq of the PyMT/GPx2 KD versus the PyMT control tumor model, we identified an overlap in cell clustering involving six luminal-like clusters and one basal/mesenchymal-like cluster (cluster 3). Similarly, scRNA-seq of lung metastases derived from the GPx2 KD tumor unraveled several luminal-like clusters and one mesenchymal-like cluster (M-cluster) which was highly homologous to primary tumor cluster 3.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
1 Sample
Download data: XLSX
Series
Accession:
GSE215394
ID:
200215394
11.

Single cell RNA sequencing on PyMT mammary gland tumor cells

(Submitter supplied) We labeled PyMT control cells versus PyMT-GPx2 KD with GFP in vitro and then injected into mammary fat pad of mice for incubating 45 days. We then generated single cell suspension by FACS sorting from PyMT-control, GPx2 KD. 10X Genomics was used to make cDNA library. We then sequenced the samples with Illumina high throughput sequencing.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
2 Samples
Download data: CSV, TAR, XLSX
Series
Accession:
GSE152368
ID:
200152368
12.

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
13.

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
14.

Identification of stable markers of the EMT:MET process

(Submitter supplied) Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) facilitate breast cancer (BC) metastasis, however stable molecular changes that result as a consequence of these processes remain poorly defined. Therefore, we sought to identify molecular markers that could distinguish tumor cells that had completed the EMT:MET cycle in the hopes of identifying and targeting unique aspects of metastatic tumor outgrowth.Therefore, normal murine mammary gland (NMumG) cells transformed by overexpression of EGFR (NME) cells were cultured in the presence of TGF-beta1 (5 ng/ml) for 4 weeks, at which point TGF-beta1 supplementation was discontinued and the cells were allowed to recover for an additional 4 weeks (Post-TGF-Rec). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
6 Samples
Download data: CEL, TXT
Series
Accession:
GSE54491
ID:
200054491
15.

Acquisition of a hybrid E/M state is essential for tumorigenicity of basal breast cancer cells

(Submitter supplied) Using the recently described CD104+/CD44hi antigen combination we demonstrate that tumorigenicity depends on individual cells residing in a hybrid E/M state. Acquisition of this E/M hybrid state is facilitated by the differential expression of EMT- TFs, like Snail accompanied by the expression of adult stem-cell programs. Transition from the highly tumorigenic E/M state to a fully mesenchymal phenotype, achieved by constitutive ectopic expression of Zeb1, is sufficient to drive cells out of the E/M hybrid state into an extreme mesenchymal (xM) state, which is accompanied by a substantial loss of tumorigenicity and a switch from canonical to non-canonical Wnt signaling.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
16.

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
41 Samples
Download data: BEDGRAPH
Series
Accession:
GSE113289
ID:
200113289
17.

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq PDX]

(Submitter supplied) The core subunit of the COMPASS-like complex, WD Repeat Domain 5 (WDR5) has a prominent role in reprogramming and Epithelial-to-Mesenchymal transition (EMT) in different tumor types. Our evidences support a model in which WDR5 is prominent for EMT and metastasis dissemination in breast cancer patient-derived xenografts and cell lines. Moreover, WDR5 silencing abrogates TGFB pathway activation and reverts mesenchymal into epithelial phenotype, by inhibiting transcription of main master regulators of EMT (CDH2, TWIST1, SNAI1, SNAI2 and ZEB1). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9115
30 Samples
Download data: TXT
18.

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq CCL]

(Submitter supplied) The core subunit of the COMPASS-like complex, WD Repeat Domain 5 (WDR5) has a prominent role in reprogramming and Epithelial-to-Mesenchymal transition (EMT) in different tumor types. Our evidences support a model in which WDR5 is prominent for EMT and metastasis dissemination in breast cancer patient-derived xenografts and cell lines. Moreover, WDR5 silencing abrogates TGFB pathway activation and reverts mesenchymal into epithelial phenotype, by inhibiting transcription of main master regulators of EMT (CDH2, TWIST1, SNAI1, SNAI2 and ZEB1). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9115
6 Samples
Download data: TXT
19.

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [ChIP-seq]

(Submitter supplied) The core subunit of the COMPASS-like complex, WD Repeat Domain 5 (WDR5) has a prominent role in reprogramming and Epithelial-to-Mesenchymal transition (EMT) in different tumor types. Our evidences support a model in which WDR5 is prominent for EMT and metastasis dissemination in breast cancer patient-derived xenografts and cell lines. Moreover, WDR5 silencing abrogates TGFB pathway activation and reverts mesenchymal into epithelial phenotype, by inhibiting transcription of main master regulators of EMT (CDH2, TWIST1, SNAI1, SNAI2 and ZEB1). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
5 Samples
Download data: BEDGRAPH
Series
Accession:
GSE113279
ID:
200113279
20.

HDAC inhibition impedes epithelial–mesenchymal plasticity and suppresses metastatic, castration-resistant prostate cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL10361 GPL13112
17 Samples
Download data: TXT
Series
Accession:
GSE67879
ID:
200067879
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