Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Phenotypic plasticity underlies invasion and distant metastasis in ovarian cancer

ABSTRACT: Phenotypic plasticity underlies invasion and distant metastasis in ovarian cancer

PROVIDER: PRJNA793826 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17408843_1.fastq.gz	Fastqsanger.gz
	SRR17408843_2.fastq.gz	Fastqsanger.gz
	SRR17408844_1.fastq.gz	Fastqsanger.gz
	SRR17408844_2.fastq.gz	Fastqsanger.gz
	SRR17408845_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 38

Similar Datasets

Phenotypic plasticity underlies local invasion and distant metastasis in ovarian cancer

Project description:Phenotypic plasticity underlies invasion and distant metastasis in ovarian cancer

2022-01-06 | GSE192920 | GEO

Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Bulk RNA-Seq)

Project description:Phenotypic plasticity and partial EMT underlie local invasion and distant metastasis in colon cancer. CD44highEpCAMhigh and CD44highEpCAMlow RNAseq profiles of colon cancer cell lines HCT116 and SW480.

2020-07-23 | GSE154927 | GEO

Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Single cell RNA-Seq)

Project description:Phenotypic plasticity and partial EMT underlie local invasion and distant metastasis in colon cancer. CD44highEpCAMhigh and CD44highEpCAMlow single cell RNAseq profiles of colon cancer cell lines HCT116 and SW480.

2020-07-23 | GSE154930 | GEO

Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Bulk RNA-Seq)

Project description:Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Bulk RNA-Seq)

| PRJNA647892 | ENA

Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Single cell RNA-Seq)

Project description:Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Single cell RNA-Seq)

| PRJNA647895 | ENA

Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer.

Project description:Phenotypic plasticity represents the most relevant hallmark of the carcinoma cell as it bestows it with the capacity of transiently altering its morphological and functional features while en route to the metastatic site. However, the study of phenotypic plasticity is hindered by the rarity of these events within primary lesions and by the lack of experimental models. Here, we identified a subpopulation of phenotypic plastic colon cancer cells: EpCAMlo cells are motile, invasive, chemo-resistant, and highly metastatic. EpCAMlo bulk and single-cell RNAseq analysis indicated (1) enhanced Wnt/β-catenin signaling, (2) a broad spectrum of degrees of epithelial to mesenchymal transition (EMT) activation including hybrid E/M states (partial EMT) with highly plastic features, and (3) high correlation with the CMS4 subtype, accounting for colon cancer cases with poor prognosis and a pronounced stromal component. Of note, a signature of genes specifically expressed in EpCAMlo cancer cells is highly predictive of overall survival in tumors other than CMS4, thus highlighting the relevance of quasi-mesenchymal tumor cells across the spectrum of colon cancers. Enhanced Wnt and the downstream EMT activation represent key events in eliciting phenotypic plasticity along the invasive front of primary colon carcinomas. Distinct sets of epithelial and mesenchymal genes define transcriptional trajectories through which state transitions arise. pEMT cells, often earmarked by the extracellular matrix glycoprotein SPARC together with nuclear ZEB1 and β-catenin along the invasive front of primary colon carcinomas, are predicted to represent the origin of these (de)differentiation routes through biologically distinct cellular states and to underlie the phenotypic plasticity of colon cancer cells.

| S-EPMC8192123 | biostudies-literature

Phenotypic plasticity determines cancer stem cell therapeutic resistance in oral squamous cell carcinoma I

Project description:Cancer stem cells (CSCs) drive tumour spread and therapeutic resistance, and can undergo epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) to switch between epithelial and post-EMT sub-populations. Examining oral squamous cell carcinoma (OSCC), we now show that increased phenotypic plasticity, the ability to undergo EMT/MET, underlies increased CSC therapeutic resistance within both the epithelial and post-EMT sub-populations. The post-EMT CSCs that possess plasticity exhibit particularly enhanced therapeutic resistance and are defined by a CD44highEpCAMlow/-CD24+ cell surface marker profile. Treatment with TGFÎ² and retinoic acid (RA) enabled enrichment of this sub-population for therapeutic testing, through which the endoplasmic reticulum (ER) stressor and autophagy inhibitor Thapsigargin was shown to selectively target these cells. Demonstration of the link between phenotypic plasticity and therapeutic resistance, and development of an in vitro method for enrichment of a highly resistant CSC sub-population, provides an opportunity for the development of improved chemotherapeutic agents that can eliminate CSCs. The CA1 OSCC cell line was sub-cloned to derive 4 clonal sub-lines, termed pEMT-P, pEMT-S, Epi-S and Epi-P (here 18, 23, 7 and 4 respectively).

2016-01-12 | E-GEOD-74578 | biostudies-arrayexpress

Phenotypic states of leptomeningeal metastasis

Project description:Phenotypic states of leptomeningeal metastasis

| PRJNA564289 | ENA

E-cadherin suppresses invasion and promotes metastasis in multiple breast cancer models

Project description:E-cadherin (E-cad) mediates cell-cell adhesion and has been proposed to suppress both invasion and metastasis. However, invasive ductal cancers retain E-cad expression in the primary tumor, circulating tumor cells, and distant metastases. We recently demonstrated that cancer cell clusters are efficient metastatic seeds. Since clusters organize through cell-cell adhesion, we tested the requirement for E-cad in genetically engineered mouse models of luminal and basal breast cancer. Loss of E-cad increased invasion and dissemination in 3D culture and in the mammary gland. However, E-cad loss also reduced cancer cell proliferation, survival, tumor cell seeding, and metastatic outgrowth in the lungs. At the transcript level, loss of E-cad was associated with increased apoptosis. Consistent with these results, inhibition of apoptosis partially rescued the metastatic phenotype of E-cad null cancer cells. We therefore propose that E-cad is an invasion suppressor, survival factor, and metastasis promoter in invasive ductal cancers.

2019-06-24 | GSE114011 | GEO

Transcriptional Coupling of Distant Regulatory Genes in Living Embryos

Project description:The prevailing view of metazoan gene regulation is that individual genes are independently regulated by their own dedicated sets of transcriptional enhancers. Past studies reported long-range gene-gene associations, but their functional significance in regulating transcription remains uncertain and controversial. Here we employ quantitative single cell live imaging methods to provide the first demonstration of co-dependent transcriptional dynamics of genes separated by large genomic distances in living embryos. We find extensive physical and functional associations of distant paralogous genes, including co-regulation by shared enhancers and co-transcriptional bursting over distances of nearly 250kb. Regulatory inter-connectivity depends on promoter-proximal tethering elements and perturbations in these elements uncouple transcription and alter the bursting dynamics of distant genes, suggesting a role of genome topology in the formation and stability of co-transcriptional hubs. Transcriptional coupling of distant genes throughout the Drosophila genome underlies a broad spectrum of conserved developmental processes, suggesting a general strategy for long-range integration of gene activities.

2022-02-01 | GSE173518 | 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