Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing results of EMT and CSC phenotypes induced by modulated expression of wild-type and mutated PSPC1 and PTK6

ABSTRACT: RNA sequencing results of EMT and CSC phenotypes induced by modulated expression of wild-type and mutated PSPC1 and PTK6

PROVIDER: PRJNA472874 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7212530_1.fastq.gz	Fastqsanger.gz
	SRR7212530_2.fastq.gz	Fastqsanger.gz
	SRR7212531_1.fastq.gz	Fastqsanger.gz
	SRR7212531_2.fastq.gz	Fastqsanger.gz
	SRR7212532_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

RNA sequencing results of EMT and CSC phenotypes induced by modulated expression of wild-type and mutated PSPC1 and PTK6

Project description:We found that PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. To elucidate mechanisms that the underlying post-translational modification of PSPC1, we performed the RNA-seq analysis of overexpression of PSPC1, alone and with PTK6, and PSPC1 tyrosine residue mutation in SK-Hep1 cells. We performed c-terminal of PSPC1 and its mutated nuclear localization site (NLS) in Mahlavu cells to evaluate its inhibitory effects on gene expression. Moreover, we further treated with HGF in Huh-7 cells to examineThe role of downstream signaling pathways of the PSPC1 and PTK6 regulation in microenviroment.

2019-05-22 | GSE114856 | GEO

RNA sequencing (RNA-SEQ) of PSPC1 knockdown by shRNA in A549 cells

Project description:We show that PSPC1 is required for cancer cell motilities and stemness properties in vitro and lung metastasis in vivo. We used high throughput sequencing to analyze the PSPC1 regulated gene expression. Loss of PSPC1 results in significant gene expression level changes in thousands of individual transcripts in key regulators of the EMT, CSCs and TGFb signaling.

2018-02-02 | GSE65523 | GEO

RNA sequencing results of cell migration and adhesion induced by modulated expression of paraspeckle protein PSPC1

Project description:We found that PSPC1 potent facilitates HCC cells motility, adhesion, cytoskeleton assembling as well as cell spreading. To elucidate underlying mechanisms regulation by PSPC1, we performed the RNA-seq analysis of overexpression of PSPC1 in SK-Hep1 cell line and knockdown od PSPC1 in Hep3B cell line to evaluate its effects on gene expression.

2020-04-14 | GSE148551 | GEO

RNA sequencing (RNA-SEQ) of PSPC1 Knockout in A549 cells with TGFb1 stimulation

2018-04-10 | GSE103293 | GEO

Identification of enhancers in EMT and breast cancer stem cell formation

2016-03-10 | E-GEOD-76732 | biostudies-arrayexpress

Identification of enhancers in EMT and breast cancer stem cell formation

2016-03-10 | GSE76732 | GEO

Identification of chromatin accessibility domains in EMT and breast cancer stem cell formation.

Project description:Epithelial-mesenchymal transition (EMT), the process whereby cells gain migratory and invasive properties characteristic of mesenchymal cells, plays a central role in embryogenesis and wound healing in a wide range of tissues. However, EMT has also been linked to the formation of cancer stem cells (CSCs). Many of the signaling pathways involved in EMT have also been implicated in CSC formation but the processes that contribute uniquely to CSC formation remain elusive. We have previously demonstrated that PKCÎ¸ activation is critical for EMT induction and concomitant CSC formation in the breast cancer luminal epithelial cell line, MCF7. To discover how PKC-induced alterations in the epigenome influence the EMT and CSC formation in MCF-7 cells, we employed a combination of expression profiling and Formaldehyde Assisted Regulatory Elements (FAIRE)-sequencing in order to reveal novel links between gene expression and DNA accessibility changes after PKCÎ¸ activation. We found that, during EMT, increases in accessibility generally occurred in regions away from transcription start sites, low in CpG, enriched with chromatin marks of enhancer elements and motifs for FOX, AP1, TEAD and AP2. Increases in FOX and AP-1 motif accessibility were associated with genes that exhibited increased expression in CSC, while increased AP-2 accessibility was associated with genes that had higher expression in non-CSCs. This study revealed novel regions of DNA accessibility induced by PKC that contribute to the understanding of how epigenomic plasticity of cells undergoing EMT leads to the activation of genes that drive the CSC program. 2 biological samples were analysed with 2 biological replicates each and a mixed total input.

2016-03-10 | E-GEOD-71023 | biostudies-arrayexpress

RNA sequencing results of cell migration and adhesion induced by modulated expression of paraspeckle protein PSPC1

Project description:RNA sequencing results of cell migration and adhesion induced by modulated expression of paraspeckle protein PSPC1

| PRJNA625033 | ENA

Transcriptome of Knockdown Pspc1 in the MS1 pancreatic islet endothelial cell line

Project description:Specific knockout Pspc1 in mouse endothelial cells cause neonatal death with multiple defects related to vascular development. The transcriptome of Pspc1 knockdown in MS1 cells corresponded to the findings from in-vivo model and reveal dampened signaling pathways.

2022-06-16 | GSE205995 | GEO

Identification of chromatin accessibility domains in EMT and breast cancer stem cell formation.

Project description:Epithelial-mesenchymal transition (EMT), the process whereby cells gain migratory and invasive properties characteristic of mesenchymal cells, plays a central role in embryogenesis and wound healing in a wide range of tissues. However, EMT has also been linked to the formation of cancer stem cells (CSCs). Many of the signaling pathways involved in EMT have also been implicated in CSC formation but the processes that contribute uniquely to CSC formation remain elusive. We have previously demonstrated that PKCθ activation is critical for EMT induction and concomitant CSC formation in the breast cancer luminal epithelial cell line, MCF7. To discover how PKC-induced alterations in the epigenome influence the EMT and CSC formation in MCF-7 cells, we employed a combination of expression profiling and Formaldehyde Assisted Regulatory Elements (FAIRE)-sequencing in order to reveal novel links between gene expression and DNA accessibility changes after PKCθ activation. We found that, during EMT, increases in accessibility generally occurred in regions away from transcription start sites, low in CpG, enriched with chromatin marks of enhancer elements and motifs for FOX, AP1, TEAD and AP2. Increases in FOX and AP-1 motif accessibility were associated with genes that exhibited increased expression in CSC, while increased AP-2 accessibility was associated with genes that had higher expression in non-CSCs. This study revealed novel regions of DNA accessibility induced by PKC that contribute to the understanding of how epigenomic plasticity of cells undergoing EMT leads to the activation of genes that drive the CSC program.

2016-03-10 | GSE71023 | 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