Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA methylation profile of model breast cancer cell lines PMC42-ET and PMC42-LA

ABSTRACT: The epithelial to mesenchymal transition (EMT), and the reverse process mesenchymal to epithelial transition (MET) is a fundamental biological process that governs embryonic development and patterning. This exquisitely-controlled phenotypic switch between two very different cellular phenotypes is commandeered in a wide range of cancers, and is considered by many to be the initiating molecular event that drives carcinoma metastasis. Because the majority of cancer-related deaths are due to metastatic spread and secondary tumour formation, elucidating the molecular mechanisms governing EMT and MET in metastasis may hold great promise for clinical benefits. Research efforts over the last 20 (?) years have focussed predominantly on identifying individual molecules and cellular signalling cascades that drive EMT/MET. Recently developed high-throughput screening approaches have enabled rapid and comprehensive genome-wide interrogation of the genetic and epigenetic changes associated with cancer to be studied. In this study we have employed Infinium 450K methyl-bead arrays to examine the DNA methylation signatures of a unique pair of isogenic human breast cancer cell lines: The mesenchymal PMC42-ET line and an epithelial-like subline PMC42-LA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE97853 | GEO | 2017/10/31

SECONDARY ACCESSION(S): PRJNA383070

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

Selvaggio2020 - Microenvironment control of hybrid Epithelial-Mesenchymal phenotypes

Project description:Epithelial to Mesenchymal Transition (EMT) has been associated with cancer cell heterogeneity, plasticity and metastasis. It has been the subject of several modeling effort. This logical model of the EMT cellular network aims to assess microenvironmental signals controlling cancer-associated phenotypes amid the EMT continuum. Its outcomes relate to the qualitative degrees of cell adhesions by adherent junctions and focal adhesions, two features affected during EMT. Model attractors recover epithelial, mesenchymal and hybrid phenotypes, and simulations show that hybrid phenotypes may arise through independent molecular paths, involving stringent extrinsic signals. Of particular interest, model predictions and their experimental validations indicated that: 1) ECM stiffening is a prerequisite for cells overactivating FAK-SRC to upregulate SNAIL1 and acquire a mesenchymal phenotype, and 2) FAK-SRC inhibition of cell-cell contacts through the Receptor Protein Tyrosine Phosphates kappa leads to the acquisition of a full mesenchymal rather than a hybrid phenotype.

2020-06-30 | MODEL2004040001 | BioModels

MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer

Project description:This SuperSeries is composed of the following subset Series: GSE39356: MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (mRNA dataset) GSE39358: MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (miRNA dataset) Refer to individual Series

2012-07-13 | E-GEOD-39359 | biostudies-arrayexpress

Expression profile from PCE-Epi and derived cell lines

Project description:To study the mechanisms of the epithelial-mesenchymal transition (EMT) in prostate cancer metastasis, we first generated an epithelial model cell line derived from prostate cancer epithelial PC3 cells. We isolated a subpopulation of cells that showed a stable epithelial phenotype in culture and designated them PC3-Epi. We next developed mesenchymal cell lines from PC3-Epi cells, through interactions with macrophages. These mesenchymal cell lines were designated PC3-EMT1, PC3-EMT12 and PC3-EMT14. We transfected two of these mesenchymal lines (PC3-EMT1 and PC3-EMT14) with lentiviral ZEB1-shRNA vector (sh4) or the scrambled control (Scr). Consistent with ZEB1's role in EMT and maintenance of the mesenchymal state, silencing of ZEB1 induced the mesenchymal-epithelial transition (MET) in PC3-EMT1 and PC3-EMT14. Cells were plated and allowed to recover for 2 days prior to RNA extraction. PC3-Epi served as a reference sample.

2013-06-14 | E-GEOD-43489 | biostudies-arrayexpress

Expression data of ALDH+ breast cancer cells

Project description:It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse. Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations. Based on established breast cancer cell lines, as well as primary tumor samples and xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites. Breast cancer cells from patient were sorted using flow cytometry to select for cells that were ALDH+. Gene expression profiles of these cells were compared with profiles of ALDH- cells.

2013-11-14 | E-GEOD-52327 | biostudies-arrayexpress

N-glycoprotein capture mass spectrometry identifies candidate substrates of human Fut enzymes

Project description:How disseminated tumor cells (DTCs) engage specific stromal components in distant organs for survival and outgrowth is a critical but poorly understood step of the metastatic cascade. Previous studies have demonstrated the importance of the epithelial-mesenchymal transition (EMT) in promoting the cancer stem cell properties needed for metastasis initiation, while the reverse process of mesenchymal-epithelial transition (MET) is required for metastatic outgrowth. Here we report that this paradoxical requirement for simultaneous induction of both MET and cancer stem cell traits in DTCs is provided by bone vascular niche E-selectin. Using cell surface alkoxyamine-biotinylation and label-free LC-MS/MS, Glg1 was identified as a top candidate Fut3/Fut6-dependent E-selectin ligand. We functionally validated their involvement in the formation of bone metastasis. These findings provide unique insights into the functional role of E-selectin as a component of the vascular niche criticalfor metastatic colonization in bone.

2019-11-13 | PXD012942 | Pride

STAT3 phosphorylation at Ser727 and Tyr705 differentially regulates the EMT-MET switch and cancer metastasis

Project description:Epithelial-mesenchymal transition (EMT)/mesenchymal-epithelial transition (MET) processes are proposed to be a driving force of cancer metastasis. By studying metastasis in bone marrow-derived mesenchymal stem cell (BM-MSC)-driven lung cancer models, microarray time-series data analysis by systems biology approaches revealed BM-MSC-induced signaling triggers early dissemination of CD133+/CD83+ cancer stem cells (CSCs) from primary sites shortly after STAT3 activation but promotes proliferation towards secondary sites. The switch from migration to proliferation was regulated by BM-MSC-secreted LIF and activated LIFR/p-ERK/pS727-STAT3 signaling to promote early disseminated cancer cells MET and premetastatic niche formation. Then, tumor-tropic BM-MSCs circulated to primary sites and triggered CD151+/CD38+ cells acquiring EMT-associated CSC properties through IL6R/pY705-STAT3 signaling to promote tumor initiation and were also attracted by and migrated towards the premetastatic niche. In summary, STAT3 phosphorylation at tyrosine 705 and serine 727 differentially regulates the EMT-MET switch within the distinct molecular subtypes of CSCs to complete the metastatic process.

2020-10-01 | GSE158824 | GEO

A critical role of histone deacetylases, Mbd3/NuRD and Tet2 in epithelial-mesenchymal cell plasticity and in tumor invasion and metastasis

Project description:We have generated and employed reversible and irreversible EMT models of murine breast cancer cells to identify the key players establishing cell state transitions during a reversible and an irreversible EMT. We demonstrate that the Mbd3/NuRD complex, involving histone deacetylases (HDACs) and Tet2 hydroxylase, acts as an epigenetic block in epithelial-mesenchymal plasticity. These epigenetic modifiers keep breast cancer cells in a stable mesenchymal state, and their pharmacological inhibition or genetic ablation leads to a mesenchymal-epithelial transition (MET) and represses primary tumor growth and metastasis formation of highly aggressive, mesenchymal breast cancer cells.

2020-04-10 | GSE100553 | GEO

Expression data of CD24-CD44+ and ALDH+ cells

Project description:It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse. Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations. Based on established breast cancer cell lines, as well as primary tumor xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites. Breast cancer cell lines, primary xenografts and normal breast cells from patient were sorted using flow cytometry to select for cells that were CD24-,CD44+ and ALDH+. Gene expression profiles of CD24-CD44+ cells were compared with non-CD24-CD44+ cells. Gene expression profiles of ALDH+ cells were compared with ALDH- cells.

2013-11-13 | E-GEOD-52262 | biostudies-arrayexpress

Expression profile from PCE-Epi and derived cell lines

2013-06-14 | GSE43489 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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