Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiRNA expression in high migratory cells

ABSTRACT: microRNAs are small non-coding RNAs, which promote either mRNAs degradation or block their translation through binding to partially complementary sequences of their target mRNAs. We have previously isolated a subpopulation with accelerated baseline motility (MG cells) or an immotile one (non-MG cells) from a colon cancer cell line (HCT116). In this study, using these subpopulations, we identified miRNAs, which were involved in acquisition of a cell migratory phenotype.

ORGANISM(S): Homo sapiens

PROVIDER: GSE141240 | GEO | 2020/02/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression of 5-azacytidine-treated HCT116 cells

Project description:DNA methylation plays an important role in regulating gene expression. In this study, a subpopulation with accelerated baseline motility (MG cells) or an immotile one (non-MG cells) from a colon cancer cell line (HCT116) were isolated, and gene expression levels of these cells with 5-azacytidine were measured by microarray analysis.

2018-12-26 | GSE114681 | GEO

Global methylation analysis of highly motility cells

Project description:Cell movement is an important character during epithelial-mesenchymal transition. A subpopulation with accelerated baseline motility (MG cells) or an immotile one (non-MG cells) from a colon cancer cell line (HCT116) were isolated. In this study, to investigate changes of global DNA methylation status between these two subpopulations, genomic DNA from these cells were subjected to DNA methylation array.

2018-12-26 | GSE114683 | GEO

Gene expression profiles of migratory and non-migratory B-cells exposed to breast cancer cell derived conditioned medium with and with extracellular vesicles

Project description:Gene expression profiles were generated using RNA-sequencing from migratory and non-migratory B-cells after exposure to conditioned medium of breast cancer cells, either containing or depleted from extracellular vesicles. The purpose of the experiment was to investigate how breast cancer cell derived extracellular vesicles induce specific molecular pathways involved in B-cell migration and B-cell infiltration.

2023-06-30 | E-MTAB-12362 | biostudies-arrayexpress

Transcriptional signature in liver reveal seasonal metabolic adaptation in the night-migratory blackheaded buntings

Project description:Purpose: Next-generation sequencing (NGS) has provided an opportunity to understand the underline processes invloved in migratory behavior. The goals of this study are to compare NGS-derived liver transcriptome profiling (RNA-seq) under migratory and non-migratory processes and understand the processes contributign under the physiological state.

2018-12-26 | GSE104748 | GEO

Carboxypeptidase E transmits its anti-migratory function in glioma cells via transcriptional regulation of cell architecture and motility regulating factors.

Project description:They aim of the study is to identify targets of Carboxypeptidase E (CPE) as well as signaling cascades that are affected by CPE which are specific for transmitting its anti-migratory effects in glioma cells by overexpressing CPE and using transcriptomics profiling of mRNAs and microRNAs.

2017-11-29 | E-MTAB-5297 | biostudies-arrayexpress

Carboxypeptidase E transmits its anti-migratory function in glioma cells via transcriptional regulation of cell architecture and motility regulating factors.

2017-11-29 | E-MTAB-5299 | biostudies-arrayexpress

Identification of a human airway epithelial cell subpopulation with altered biophysical, molecular, and metastatic properties

Project description:Lung cancers are documented to have remarkable intratumoral genetic heterogeneity. However, little is known about the heterogeneity of biophysical properties, such as cell motility, and its relationship to early disease pathogenesis and micrometastatic dissemination. In this study, we identified and selected a subpopulation of highly migratory premalignant pulmonary epithelial cells that were observed to migrate through microscale constrictions at up to 100-fold the rate of unselected cells. This enhanced migratory capacity was found to be Rac1-dependent and heritable, as evidenced by maintenance of the phenotype through multiple cell divisions continuing more than 8-weeks post-selection. The morphology of this lung epithelial subpopulation was characterized by increased cell protrusion intensity. In a murine model of micrometastatic seeding and pulmonary colonization, the motility-selected premalignant cells exhibit both enhanced survival in short term assays and enhanced outgrowth of premalignant lesions in longer term assays, thus overcoming important aspects of “metastatic inefficiency.” Overall, our findings indicate that among premalignant pulmonary epithelial cells, subpopulations with heritable motility-related biophysical properties exist, and these may explain micrometastatic seeding occurring early in the pathogenesis of lung cancer. Understanding, targeting, and preventing these critical biophysical traits and their underlying molecular mechanisms may provide a new approach to prevent metastatic behavior.

2017-06-28 | GSE100527 | GEO

Transcription profiling of Drosophila of wild type migratory border cells (WTBC), non-migrating slbo mutant border cells (slboBC) and non-migrating follicle cells (FC)

Project description:Expression profiles of wild type migratory border cells (WTBC), non-migrating slbo mutant border cells (slboBC) and non-migrating follicle cells (FC)

2006-04-01 | E-MEXP-493 | biostudies-arrayexpress

miRNA expression in high migratory cells

Project description:miRNA expression in high migratory cells

| PRJNA592907 | ENA

A Suv39H1-low chromatin state drives migratory cell populations in cervical cancer [ChIP-Seq]

Project description:The evolution of migratory populations of cells within solid tumours represents a critical stage during cancer metastasis. We have previously reported the enhanced migratory properties of one such population, marked by the expression of CD66, within cervical cancers. However, it is not clear what mechanisms drive such migratory populations, and how these cells would retain a “memory” of initial migration-inducing cues during metastasis. Here, we describe the role of a Suv39H1-low heterochromatin state as a driver of cervical cancer migratory populations. Cervical cancer cells were sorted based on migratory ability in vitro. These migrated populations show low Suv39H1, and Suv39H1 knockdown enhances cell migration. Using histopathology to examine clinical carcinoma progression, initial progression showed expansion of a proliferative Suv39H1high population, followed by the emergence of a sarcomatoid, migratory Suv39H1low cell population in advanced stages. Additionally, meta-analysis of TCGA data revealed that low tumoural Suv39H1 also correlated with lower patient survival, and with expression signatures of migration, TGF-β signalling, and links with a CD66 cell signature. Lastly, using RNA-Seq and H3K9me3 ChIP-Seq on migrated populations in vitro, it was observed that these populations show Suv39H1-linked transcriptome alterations and broad scale H3K9me3 remodelling. This Suv39H1-linked heterochromatin regulation could explain plasticity in migratory and metastatic populations, and allows for a “memory” of migration inducing cues, through metastable changes in chromatin conformation. The understanding of such regulatory mechanisms in migratory populations may prove valuable in efforts to develop anti-metastatic strategies.

2019-03-01 | GSE103793 | 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