Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-Cell RNA-Sequencing reveals cellular heterogeneity and trajectories of lineage specification of mammary basal epithelial cells of WT and Fgd5-depeleted mice

ABSTRACT: Single-Cell RNA-Sequencing reveals cellular heterogeneity and trajectories of lineage specification of mammary basal epithelial cells of WT and Fgd5-depeleted mice

PROVIDER: PRJNA857692 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR20079643_1.fastq.gz	Fastqsanger.gz
	SRR20079643_2.fastq.gz	Fastqsanger.gz
	SRR20079644_1.fastq.gz	Fastqsanger.gz
	SRR20079644_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Single-Cell RNA-Sequencing reveals cellular heterogeneity and trajectories of lineage specification of mammary basal epithelial cells of WT and Fgd5-depeleted mice

Project description:We report the application of Single-Cell RNA-Sequencing technology for high-throughput profiling in mammary basal epithelial cells of WT and Fgd5-depeleted mice. By obtaining basal epithelial cells isolated from mammary gland of WT and Fgd5-depeleted mice, we performed Single-Cell RNA-Sequencing of basal epithelial cells. The scRNA-Seq libraries were prepared with Single Cell 3′ Reagent Kit v2 (10×Genomics) following the user guide provided. We found that FGD5 promotes mammary development by maintaining LGR5/SLPI/ID3 positive basal cell subsets.. We conclude that Single-Cell RNA-Sequencing would expedite genetic network analyses and permit the dissection of complex biologic functions.

2022-10-08 | GSE207922 | GEO

Single cell transcriptomics reveals involution mimicry during the specification of the basal breast cancer subtype

Project description:Here, we use spatially and time controlled induction of Elf5 within the mammary epithelium in the context of the luminal MMTV-PyMT mouse mammary cancer to study tumour progression mechanisms associated to the specification of the basal breast cancer subtype at single-cell resolution.

2021-03-05 | GSE158677 | GEO

The effect of macrophage depletion on mammary basal cells

Project description:To investigate the effect of macrophages on mammary basal cells, we established a macrophage depletion mouse model by clodronate liposome (CL) intraperitoneal injection, and the mammary basal cells were collected by FACS sorting. We then performed RNA-seq analysis on clodronate liposome (CL) treated mammary basal cells compared to control.

2023-04-20 | GSE210268 | GEO

VE-PTP inhibition stabilizes endothelial junctions by activating FGD5

Project description:Inhibition of VE-PTP, an endothelial receptor type tyrosine phosphatase, triggers phosphorylation of the tyrosine kinase receptor Tie-2, which leads to the suppression of inflammation-induced vascular permeability. Analyzing the underlying mechanism, we show here that inhibition of VE-PTP and activation of Tie-2 induce tyrosine phosphorylation of FGD5, a GTPase exchange factor (GEF) for Cdc42, and stimulate translocation of this GEF to cell contacts. Interfering with the expression of FGD5 blocked the junction stabilizing effect of VE-PTP inhibition in vitro and in vivo. Likewise, FGD5 was required for strengthening of cortical actin bundles and inhibiting radial stress fiber formation, which were each stimulated by VE-PTP inhibition. We identified Y820 of FGD5 as the direct substrate for VE-PTP. Inhibition of VE-PTP could no longer stabilize endothelial junctions or activate Cdc42 if endothelial cells expressed a Y820F point mutated version of FGD5. In contrast, FGD5-Y820F was still recruited to endothelial cell contacts. Thus, activation of FGD5 is a two-step process that comprises membrane recruitment and phosphorylation of Y820. These steps are necessary for the junction stabilizing effect that is stimulated by VE-PTP inhibition and Tie-2 activation.

2019-05-04 | PXD010959 | Pride

Expression data from MM231 and MM231-FGD5-cas9 breast cancer cells

Project description:To identify the differiational genes and pathways in MM231 and MM231-FGD5-cas9, we examined the microarray gene expression profile of MM231 breast cancer cells vs FGD5-cas9 cells. Ectopic expression or activation of EGFR is found in most TNBCs, and EGFR inhibitors can suppress TNBC growth in vitro. However, these agents exhibit limited efficacy in TNBC patients, possibly due to the nonkinase oncogenic functions of EGFR and the compensatory effects of other oncogenic activities following anti-EGFR therapy. Here, we identified a positive correlation between EGFR and FGD5 expression in TNBC samples. FGD5 deletion attenuated TNBC initiation and progression by decreasing EGFR stability and expression. Moreover, the proteins involved in mutual compensation of EGFR signaling were significantly downregulated in FGD5-deleted TNBC cells. Mechanistically, FGD5 interacted with EGFR to maintain EGFR stability by impeding EGFR ubiquitylation and degradation mediated by the E3 ligase ITCH; disrupting the FGD5-EGFR interaction accelerated EGFR degradation and produced robust anti-TNBC activity. Our study shows that targeted degradation of EGFR through disrupting the FGD5-EGFR interaction is a promising therapeutic strategy for the TNBC subtype of breast cancer.

2020-01-27 | GSE144260 | GEO

Positional cues underlie cell fate specification during branching morphogenesis of the embryonic mammary epithelium

Project description:By single-cell RNA-sequencing across 4 stages of embryonic development, we reconstructed the differentiation trajectories of multipotent mammary stem cells towards basal and luminal fate. Our data revealed that MaSCs can already be resolved into distinct populations exhibiting lineage commitment at the time coinciding with the first sprouting events of mammary branching morphogenesis (E15.5). Through an interactive web tool for the visualization of gene expression across our developmental atlas, we provide novel molecular markers for committed and multipotent MaSCs, and define their spatial distribution within the developing tissue. Furthermore, we show that the mammary embryonic mesenchyme is composed of two spatially-restricted cell populations, representing the sub-epithelial and dermal mesenchyme.

2024-02-05 | GSE210594 | GEO

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Project description:Basal breast cancers, an aggressive breast cancer subtype that has poor treatment options, are thought to arise from luminal mammary epithelial cells that undergo basal-like plasticity through poorly understood mechanisms. Using genetic mouse models and ex vivo primary organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effectors of Hippo pathway signaling, in mature mammary luminal epithelial cells promotes the development of basal-like carcinomas that metastasize over time. Genetic co-deletion experiments revealed that phenotypes resulting from the loss of LATS1/2 activity are dependent on the transcriptional regulators YAP/TAZ. Notably, transcriptional analyses of LATS1/2-deleted mammary epithelial cells revealed a gene expression program that associates with human basal breast cancers. Our study demonstrates in vivo roles for the LATS1/2 kinases in mammary epithelial homeostasis and luminal-basal fate control and implicates signaling networks induced upon the loss of LATS1/2 activity in the development of basal breast cancers.

2022-09-26 | GSE196555 | GEO

Effect of laminin adhesion on basal human mammary epithelial cells

Project description:Mammary epithelium is composed by luminal and basal epithelial cells, which are adhere to the basement membrane (BM). To dissect how basal cell functions are regulated by BM laminin adhesion, we performed RNA sequencing of basal human mammary epithelial cells adhered on laminin-111, -421 or -521 coated cell culture plates for 48 hours.

2022-11-07 | GSE197950 | GEO

Transcription Factor RFX3 Stabilizes Mammary Basal Cell Identity

Project description:Transcription Factor RFX3 Stabilizes Mammary Basal Cell Identity

| PRJNA790932 | ENA

Transcriptome analysis of Scramble control and Cdk14-sh mouse mammary basal cells

Project description:Wnt/β-catenin signaling pathway has become a key signaling pathway regulating mammary organogenesis and oncogenesis. However, the therapeutic methods by targeting Wnt pathway against breast cancer has been limited. To address this challenge, we investigated the function of cyclin-dependent kinase 14 (CDK14), a member of Wnt signaling pathway, in mammary development and breast cancer progression. We showed that CDK14 was expressed in the mammary basal layer and elevated in triple negative breast cancer (TNBC). CDK14 knockdown reduces colony formation ability and regeneration capacity of mammary basal cells, and significantly inhibits murine MMTV-Wnt-1 basal-like mammary tumor progression. Excitingly, knockdown of CDK14 or pharmacological inhibition of CDK14 by FMF-04-159-2 significantly inhibited the progression and metastasis of human TNBC. Mechanistically, CDK14 inhibition inhibits mammary regeneration and TNBC progression by attenuating Wnt/β-catenin signaling. Together, we demonstrated that CDK14 regulates mammary regeneration and breast tumorigenesis, and is a promising therapeutic target for TNBC.

2022-04-29 | GSE201526 | 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