Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epithelial-mesenchymal plasticity induced by discontinuous exposure to TGFβ1 increases tumorigenic potential of normal epithelial cells

ABSTRACT: Epithelial-mesenchymal plasticity induced by discontinuous exposure to TGFβ1 increases tumorigenic potential of normal epithelial cells

PROVIDER: PRJNA750402 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15278018_1.fastq.gz	Fastqsanger.gz
	SRR15278018_2.fastq.gz	Fastqsanger.gz
	SRR15278019.fastq.gz	Fastqsanger.gz
	SRR15278019_1.fastq.gz	Fastqsanger.gz
	SRR15278019_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 17

Similar Datasets

Epithelial-mesenchymal plasticity induced by discontinuous exposure to TGFβ1 increases tumorigenic potential of normal epithelial cells

Project description:In this manuscript, we used a non-genetically manipulated EMT/MET cell line model to demonstrate that epithelial mesenchymal plasticity occurring in normal cells generates co-existing phenotypically and functionally divergent cell subpopulations with increased tumorigenic potential in vivo.

2021-07-30 | GSE181008 | GEO

TGFβ1 treatment of A2058 melanoma cells

Project description:4 replicates were prepared from A2058 melanoma cells [transfected with 10ng of empty vector (pcDNA3.1+)] and treated with 5ng/ml TGFβ1 or vehicle control for 24hrs This is the control arm of a larger experiment where cells transfected with a particular expression plasmid were treated with TGFβ1 or control vehicle. The transfection with the expresion plasmid was unsucessful so this empty vector data has been used alone to simply examine the effect of TGFβ1 treatment on A2058 cells.

2015-02-20 | E-GEOD-66114 | biostudies-arrayexpress

TGFβ1 promotes collective invasion of oncogenically transformed intestinal organoids by inducing partial epithelial-mesenchymal transition independently of Snail1 and Zeb1

Project description:Cancer cells simultaneously featuring epithelial and mesenchymal traits appear particularly competent to invade and metastasize. However, genetic prerequisites and signaling pathways promoting such partial epithelial-to-mesenchymal transitions (EMT) remain obscure. Here we report that murine intestinal organoids with hyperactive Wnt and MAPK signaling, and mutant Trp53 are purely epithelial and non-invasive in vitro, but initiate a collective invasion program when treated with TGFβ1. Invasive organoids reciprocally interact with the extracellular matrix (ECM), and autonomously deposit and remodel components thereof. Although cells at the organoid/ECM interface shed certain epithelial characteristics, invasive organoids largely maintain epithelial gene expression while concomitantly upregulating a mesenchymal program. TGFβ1-induced phenotypic changes involve canonical, Smad4-dependent signaling, yet, are unimpeded by knockout of Snai1 and Zeb1 - otherwise key regulators of epithelial-to-mesenchymal transitions. The finding of TGFβ1-inducible, Snail1/Zeb1-independent collective invasion of oncogenically transformed intestinal organoids provides novel mechanistic insights and broadens the spectrum of context-dependent manifestations of partial EMT.

2022-01-24 | GSE156553 | GEO

A RNA-seq-based gene expression profiling of radiation-induced tumorigenic mammary epithelial cells

Project description:To understand tumorigenesis and cancer progression of mammary epithelium, we established a cell model combining over-expression of human telomerase reverse transcriptase gene (hTERT) and heavy-ion radiation from normal human mammary epithelial cells. We subsequently used RNA-seq method to acquire their transcriptomes from two characteristic cell lines, an immortal epithelial cell line (I_hMEC) and a tumorigenic epithelial cell line (T_hMEC), and to look for differentially expressed genes (DEGs) between immortalization and tumorigenicity. We identified 7,053 DEGs, of which 84 were not only highly expressed but also significantly regulated. We found that house-keeping (HK) genes and tissue-specific (TS) genes were regulated differently during tumorigenesis; HK genes tend to be activated but TS genes tend to be repressed. We looked into three important pathways in cancer development: p53 signaling, cell cycle, and apoptosis. Although both immortal and tumorigenic cells have infinite potential to replicate and can escape apoptosis, a great number of genes exhibited different modulation pattern between the two processes. We also found that a significant number of DEGs were involved in epigenetic modification of chromatins. In conclusion, these findings may provide novel biomarkers in studying tumorigenicity and further our understanding of cellular mechanism(s) in the transition from immortal to tumorigenic processes. 2 samples examined: immortalized human mammary epithelial cell (I_hMEC) and tumorigenic human mammary epithelial cell (T_hMEC)

2013-12-09 | E-GEOD-31310 | biostudies-arrayexpress

Tumorspheres from transformed fibroblasts highlight the great plasticity of differentiated tumorigenic cells

Project description:Tumorspheres from transformed fibroblasts highlight the great plasticity of differentiated tumorigenic cells

| PRJNA432038 | ENA

Knockdown of HSPA13 inhibits TGFβ1-induced epithelial-mesenchymal transition of RPE by suppressing the PI3K/Akt signaling pathway

Project description:To investigate the effect of HSPA13 on TGFβ1-induced EMT of RPE cells, we performed bulk RNA sequencing (RNA-seq). Gene set enrichment analysis (GSEA) revealed that gene signatures associated with EMT and cell migration were significantly downregulated in the shHSPA13+TGFβ1 group relative to the shScramble+TGFβ1 group. PI3K/Akt signaling-related gene levels were repressed as well.

2024-09-04 | GSE264212 | GEO

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

Project description:Epithelial-mesenchymal transition (EMT) fosters cancer cell invasion and metastasis, the main cause of cancer-related mortality. Growing evidence that SNAIL and ZEB transcription factors, typically portrayed as master regulators of EMT, may be dispensable for this process, led us to re-investigate its mechanistic underpinnings. For this, we used an unbiased computational ap-proach that integrated time-resolved analyses of chromatin structure and differential gene ex-pression, to predict transcriptional regulators of TGFβ1-inducible EMT in the MCF10A mam-mary epithelial cell line model. Bioinformatic analyses indicated comparatively minor contri-butions of SNAIL proteins and ZEB1 to TGFβ1-induced EMT, whereas the AP-1 subunit JUNB was anticipated to have a much larger impact. CRISPR/Cas9-mediated loss-of-function studies confirmed that TGFβ1-induced EMT proceeded independently of SNAIL proteins and ZEB1. In contrast, JUNB was necessary and sufficient for EMT in MCF10A cells, but not in A549 lung can-cer cells, indicating cell-type-specificity of JUNB EMT-regulatory capacity. Nonetheless, the JUNB-dependence of EMT-associated transcriptional reprogramming in MCF10A cells allowed to define a gene expression signature which was regulated by TGFβ1 in diverse cellular back-grounds, showed positively correlated expression with TGFβ signaling in multiple cancer tran-scriptomes, and was predictive of patient survival in several cancer types. Altogether, our find-ings provide novel mechanistic insights into the context-dependent control of TGFβ1-driven EMT and thereby may lead to improved diagnostic and therapeutic options.

2023-01-17 | GSE210499 | GEO

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

2023-01-17 | GSE210498 | GEO

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

2023-01-17 | GSE210496 | GEO

Hic-5 regulates epithelial to mesenchymal transition in ovarian cancer cells in a TGFβ1-independent manner

Project description:The molecular basis of epithelial ovarian cancer (EOC) dissemination is still poorly understood. We have previously identified the hydrogen peroxide-inducible clone-5 (Hic-5) gene as hypomethylated in high-grade (HG) serous EOC tumors, compared to normal ovarian tissues. Hic-5 is a focal adhesion scaffold protein and has been primarily studied for its role as a key mediator of TGF-β–induced epithelial-to-mesenchymal transition (EMT) in epithelial cells of both normal and malignant origin; however, its role in EOC has been never investigated. Here we demonstrate that Hic-5 is overexpressed in advanced EOC, and that Hic-5 is upregulated upon TGFβ1 treatment in the EOC cell line with epithelial morphology (A2780s), associated with EMT induction. However, ectopic expression of Hic-5 in A2780s induces alone EMT, accompanied with enhancement of their proliferation rate and migratory/invasive capacity and increased resistance to chemotherapeutic drugs. Moreover, Hic-5 knockdown in the EOC cell lines with mesenchymal morphology (SKOV3), was accompanied by induction of mesenchymal-to-epithelial transition (MET), followed by a reduction of their proliferative, migratory and invasive capacity, and increased drugs sensitivity in vitro and enhanced tumor cell colonization and metastatic growth in vivo. The modulation of Hic-5 expression in EOC cells resulted in altered regulation of numerous EMT-related canonical pathways and was indicative for a possible role of Hic-5 in controlling EMT through a RhoA/ROCK mediated mechanism. To our knowledge, this is the first report examining the role of Hic-5 in EOC, and its role in maintaining the mesenchymal phenotype of EOC cells independently of exogenous TGFβ1 treatment.

2017-10-22 | GSE98737 | 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