Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression of mammary epithelial anoikis microRNAs and target genes

ABSTRACT: Expression of mammary epithelial anoikis microRNAs and target genes

PROVIDER: PRJNA1025015 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26313720.fastq.gz	Fastqsanger.gz
	SRR26313721.fastq.gz	Fastqsanger.gz
	SRR26313722.fastq.gz	Fastqsanger.gz
	SRR26313723.fastq.gz	Fastqsanger.gz
	SRR26313724.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Differential microRNA expression in adherent versus suspended MCF10A mammary epithelial cells

Project description:The ability to survive following loss of adhesion underpins cancer metastasis and significantly contributes triple negative breast cancer (TNBC) morbidity. Epithelial cells that form solid tumors must evade anoikis, a special type of cell death that occurs upon detachment from the extracellular matrix in order to colonize in distal sites. While there have been several advances in the understanding of the mechanisms by which cells undergo anoikis, the role for noncoding RNAs (ncRNAs) in this process is less well understood. An important role for microRNAs (miRNAs) in regulating anoikis is beginning to emerge, however in general the mechanisms by which miRNAs regulate anoikis are largely unknown. Thus we utilized the anoikis-sensitive immortalized mammary epithelial cell line, MCF10A to unbiasedly determine the microRNAs differentially regulated upon detachment.

2023-10-30 | GSE244857 | GEO

JNK promotes epithelial cells anoikis by transcriptional and post-translational regulation of BH3-only proteins

Project description:Developmental morphogenesis, tissue injury, and oncogenic transformation can cause the detachment of epithelial cells. These cells are eliminated by a specialized form of apoptosis (anoikis). While the processes that contribute to this form of cell death have been studied, the underlying mechanisms remain unclear. Here we tested the role of the cJUN NH2-terminal kinase (JNK) signaling pathway using murine models with compound JNK-deficiency in mammary and kidney epithelial cells. These studies demonstrated that JNK is required for efficient anoikis in vitro and in vivo. Moreover, JNK-promoted anoikis required pro-apoptotic members of the BCL2 family of proteins. We show that JNK acts through a BAK/BAX-dependent apoptotic pathway by increasing BIM expression and phosphorylating BMF leading to death of detached epithelial cells.

2017-11-14 | GSE88856 | GEO

Expression of mammary epithelial anoikis microRNAs and target genes

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-30 | GSE244859 | GEO

Bovine mammary epithelial cells in response to artemisinin treatment

Project description:Bovine mammary epithelial cells in response to artemisinin treatment

2020-09-02 | PXD021269 |

Mammary Epithelial Subsets by Cell Cycle

Project description:Human mammary epithelial cells sorted by cell cycle

2022-04-07 | MSV000089219 | MassIVE

Mammary epithelial cells have lineage-rooted metabolic identities

Project description:Global proteomic profiling of three mammary epithelial cell types in normal human breast tissue. Primary breast specimens were obtained from 10 women undergoing reduction mammoplasties. Clinical co-variates include age (28-67), hormone status (follicular, luteal, post-menopausal) and mammary epithelial cell type (basal, luminal progenitor, mature luminal).

2021-03-12 | MSV000087042 | MassIVE

Gene expression profiles induced by knockdown and overexpression of p63 variants in MCF-10A mammary epithelial cell line

Project description:p63 is critical for epithelial development yet little is known about the transcriptional programmes it regulates. The p63 transactivating (TA) isoforms contain an amino-terminal exon that encodes a p53-like transactivation domain, whereas ΔN-isoforms lack this domain but contain the common DNA binding domain (DBD), suggesting that TAp63 and ΔNp63 isoforms may have opposing functions. By characterising transcriptional changes and cellular effects following modulation of p63 expression, we have defined a vital role for p63 in cellular adhesion. Knockdown of p63 expression caused downregulation of cell adhesion-associated genes, cell detachment and anoikis in mammary epithelial cells and keratinocytes. Conversely, overexpression of the TAp63γ or ΔNp63α isoforms of p63 upregulated cell adhesion molecules, increased cellular adhesion and conferred resistance to anoikis.

2010-03-12 | GSE20286 | GEO

Expression array of mammary epithelial cells isolated from epithelial Mmp14-targeted mammary glands

Project description:Mammary gland branching morphogenesis is thought to relie on the mobilization of the membrane-anchored matrix metalloproteinase, Mmp14/MT1-MMP, to drive mammary epithelial invasion by remodeling the extracellular matrix and triggering associated signaling cascades. However, the roles that this proteinase plays during postnatal mammary gland development in vivo remain undefined. A mammary gland branching program that occurs during the first 4 weeks of postnatal mouse development, in tandem with recently developed Mmp14-floxed mice and MMTV-Cre transgenics that express Cre recombinase throughout the mammary epithelial cell compartment, were used to characterize the impact of deleting epithelial cell Mmp14 on mammary gland morphogenesis. Transcriptome profiling of mammary epithelial cells was used to investigate the functional roles of MT1-MMP in the postnatal mammary epithelial cell compartment in an unbiased fashion

2018-12-01 | GSE118465 | GEO

Expression array of mammary epithelial cells isolated from epithelial Mmp14-targeted mammary glands

Project description:Expression array of mammary epithelial cells isolated from epithelial Mmp14-targeted mammary glands

| PRJNA485735 | ENA

A microRNA/circle RNA axis promotes metastasis through CDR1-mediated anoikis-resistance

Project description:Lung cancer is an intrinsically highly metastatic disease and the leading cause of cancer-related deaths worldwide. Although discovery of molecular aberrations in lung adenocarcinomas has led to development of effective targeted therapies, corresponding “drivers” in lung squamous carcinomas (LUSC) have not materialized. Extensive molecular profiling has revealed LUSC tumors have non-recurrent somatic mutations and are largely driven by copy number alterations. Because microRNAs (miRs) play increasingly important roles in regulating metastasis-relevant pathways, we evaluated whether miRs can regulate LUSC progression. By integrating bioinformatics of the Cancer Genome Atlas (TCGA) with novel, highly metastatic LUSC models, we found that miR-671-5p is a key inhibitor of LUSC metastasis. Surprisingly, miR-671-5p regulates LUSC metastasis by inhibiting a circular RNA (circRNA), CDR1as. Although the putative function of CDR1as is through miR-7 sponging, we found miR-671-5p more potently silences an axis of CDR1as and its anti-sense transcript, cerebellar degeneration related antigen 1 (CDR1). To our knowledge, no function of CDR1 has ever been described. We found loss of CDR1as and CDR1 significantly inhibited LUSC metastases. Intriguingly, CDR1 was strongly associated with an epithelial-mesenchymal transition (EMT) program in LUSC tumors, and was sufficient to promote metastases, increased migration and substrate-independent survival, known as anoikis-resistance. CDR1, which directly interacts with AP1 and COPI subunits, no longer promoted migration and anoikis-resistance upon blockade of Golgi trafficking. Our findings reveal a miR/circRNA axis that regulates LUSC metastases through an enigmatic protein, CDR1.

2021-09-08 | PXD012286 | Pride

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