Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Roles of EMT regulator in colon cancer

ABSTRACT: Isolation and enrichment of cancer stem cells in colorectal carcinoma to study role of epithelial-mesenchymal transition regilators in tumor malignancy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE14773 | GEO | 2011/10/25

SECONDARY ACCESSION(S): PRJNA112159

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of human colon cancer sphere cells and parental control cells to study the role of epithelial-mesenchymal transition regulators in tumor malignancy

Project description:Isolation and enrichment of cancer stem cells in colorectal carcinoma to study role of epithelial-mesenchymal transition regilators in tumor malignancy. Experiment Overall Design: Genome-wide comparision in sphere cells and parental control cells revealed potential regulators involved tumor malignancy . Experiment Overall Design: Overexpression of these key regulators drafted cellular context toward therapy resistance

2009-10-16 | E-GEOD-14773 | biostudies-arrayexpress

Cellular and extracellular vesicle RNA sequence for E-cadherin-RFP EMT reporter system expressing mouse breast cancer cell line Py2T during EMT/MET

Project description:Epithelial-mesenchymal transition (EMT) is a process by which epithelial cells lose cell-cell contact and gain cancer malignancy such as invasion, stemness, chemoresistance and metastasis. Reverse precess, mesenchymal-epithelial transition (MET) is also important for colonization. Extracellular vesicles (EVs) secreted from cancer cells are also important for cancer malignancy. To analyze RNAs from cells and EVs during EMT and MET, RNA sequencing was performed using E-cadherin-RFP/Py2T reporter system.

2020-12-31 | E-MTAB-9750 | biostudies-arrayexpress

"High Levels of EMT-TFs for the Diagnosis of Colorectal Cancer (CRC)"

Project description:The present study is aimed at detecting and measuring mRNA levels of genes involved in epithelial to mesenchymal transition (EMT) in biological samples, i.e. in peripheral blood samples of colorectal cancer (CRC) patients and healthy controls, to determine the presence of disease, its progression and risk of recurrence.

| 2334276 | ecrin-mdr-crc

gene profiling in carcinoma cell during EMT

Project description:Modulation of several waves of gene expression during FGF-1 induced Epithelial-mesenchymal transition of carcinoma cells . In vitro FGF-1 induced EMT study using NBTII rat bladder carcinoma cells Keywords: time course ; EMT ; cancer cell line ; FGF-1

2008-02-20 | GSE5664 | GEO

ZEB2-mediated EMT in CRC cell line DLD-1

Project description:We report the induction of epithelial-mesenchymal transition (EMT) in the epithelial colorectal cancer (CRC) cell line DLD-1. ZEB2 expression is sufficient to induce the downregulation of epithelial markers such as E-cadherin, claudins, keratins and occludins, while upregulating the expression of several mesenchymal markers as vimentin and fibronectin.

2020-04-18 | GSE148823 | GEO

Proteome landscape of epithelial to mesenchymal transition (EMT) of retinal pigment epithelium shares commonalities with malignancy-associated EMT

Project description:Retinal pigment epithelium (RPE) stress and injury often leads to epithelial to mesenchymal transition (EMT), in which RPE cells lose its cobblestone morphology and acquire more motile and spindle-shaped fibroblast phenotype. RPE dysfunction due to acquired EMT phenotype have been implicated in a number of retinal diseases such as proliferative vitreoretinopathy (PVR), diabetic retinopathy (DR), neovascular (“wet”) and atrophic (“dry”) age-related macular degeneration (AMD). We investigated distinct temporal protein expression changes and signaling events that occur during enzymatically dissociated hRPE EMT model, as well as those that occur up to forty-eight hours after EMT onset. Further, we compared analysis on altered proteome profiling with malignancy associated EMT and AMD models. Together, proteome profiles provide a comprehensive RPE EMT resources for understanding molecular signaling events, associated biological pathways, that underlie RPE-EMT onset and further identifying chemical modulators that could potentially inhibit RPE EMT.

2021-09-21 | PXD019600 | Pride

FHOD1 in EMT

Project description:Comparison of gene expression in oral squamous carcinoma cells of epithelial and mesenchymal type

2013-12-11 | E-MTAB-1420 | biostudies-arrayexpress

Trajectories of partial and full EMT of mammary tumor cells in the MMTV-PyMT mouse model

Project description:Epithelial-mesenchymal transition (EMT) is a multistep process of cell de-differentiation which confers carcinoma cells with a variety of malignant characteristics. Due to the transient and reversible nature of the process, cancer cells may transit between various stages of an EMT continuum, including epithelial, partial EMT or full EMT, and the actual status of cancer cells, the kinetics of cellular state transition in vivo and the consequences thereof have remained elusive. We have established tamoxifen inducible dual recombinase lineage tracing systems combined with live cell imaging and 5-cell RNA-sequencing analysis to track cancer cells undergoing a partial or a full EMT in the MMTV-PyMT mouse model of metastatic breast cancer. In primary tumours, cancer cells infrequently undergo an EMT, and most of these cells transition between epithelial and partial EMT states, but rarely undergo a full EMT. Consequently, cells that have ever undergone a partial EMT dynamically transit between various EMT states, and they contribute to lung metastasis and chemoresistance. In contrast, full EMT cells mostly retain a mesenchymal phenotype and stably reside in perivascular regions, but fail to colonize the lungs. However, full EMT cancer cells are enriched in recurrent tumors upon chemotherapy. Our findings suggest that cancer cells in various stages of the EMT continuum contribute differentially to hallmarks of breast cancer malignancy, such as cell migration, invasion, metastasis and chemoresistance.

2021-11-18 | GSE171940 | GEO

H2B variants expression during iAs-mediated EMT

Project description:This work details the first global mass spectrometric analysis of histone H2B variants as cells undergo arsenic-mediated epithelial to mesenchymal transition.

2016-05-17 | PXD003503 | Pride

A Wnt-induced phenotypic switch in cancer-associated fibroblasts inhibits EMT in colorectal cancer

Project description:Tumor progression is recognized as a result of an evolving crosstalk between tumor cells and their surrounding non-transformed stroma. Although Wnt signaling has been intensively studied in colorectal cancer (CRC), it remains unclear whether activity in the tumor-associated stroma contributes to malignancy. To specifically interfere with stromal signals, we generated Wnt-independent tumor organoids that secrete the Wnt antagonist Sfrp1. Upon subcutaneous transplantation into immuno-competent as well as -deficient mice, we observed strong reduction of tumor growth. Histological and transcriptomic analyses revealed that Sfrp1 induces an EMT (epithelial-mesenchymal transition) phenotype in tumor cells without affecting tumor-intrinsic Wnt signaling, suggesting involvement of non-immune stromal cells. Indeed, blockage of canonical signaling using Sfrp1, Dkk1, or fibroblast-specific genetic ablation of β-catenin strongly decreased the number of cancer-associated myofibroblasts (myCAFs). Interestingly, we found that the Wnt activity in CAFs is linked with distinct subtypes, where low and high levels induce an inflammatory-like CAF (iCAF) subtype or contractile myCAFs, respectively. Co-culture of tumor organoids with iCAFs resulted in massive upregulation of EMT markers, while myCAFs reverted this phenotype. In summary, we show that tumor growth and malignancy are differentially regulated via district fibroblast subtypes under the influence of juxtacrine Wnt signals.

2020-10-15 | GSE155364 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data