Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of CMT64 cells following TGF-β and/or TNF-α treatment.

ABSTRACT: Transcriptome analysis of CMT64 cells following TGF-β and/or TNF-α treatment.

PROVIDER: PRJNA689310 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13344611_1.fastq.gz	Fastqsanger.gz
	SRR13344611_2.fastq.gz	Fastqsanger.gz
	SRR13344612_1.fastq.gz	Fastqsanger.gz
	SRR13344612_2.fastq.gz	Fastqsanger.gz
	SRR13344613_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Transcriptome analysis of CMT64 cells following TGF-β and/or TNF-α treatment.

Project description:We have previously demonstrated that TNF-α, a proinflammatory cytokine, enhances TGF-β-mediated EMT in A549 human lung cancer cells. RNA-sequencing analysis on CMT64 cells following TGF-β and/or TNF-α treatment revealed a subset of genes possibly regulated by TGF-β and/or TNF-α.

2021-12-13 | GSE164160 | GEO

Transcriptional effects of TNF-Î± and TGF-Î²1 on human umbilical vein endothelial cells

Project description:Transcriptional profiling of human umbilical vein endothelial cells following stimulation with tumour necrosis factor alpha and transforming growth factor beta singly or combined for 8 hr All stimulations were for 8 hr - TNF-Î± vs no cytokine; TGF-Î²1 vs no cytokine; TNF-Î± & TGF-Î²1 vs TNF-Î± alone; TNF-Î± & TGF-Î²1 vs TGF-Î²1 alone

2012-10-31 | E-GEOD-33416 | biostudies-arrayexpress

TGF or TNF Time series in ARPE19

Project description:Aberrant epithelial-mesenchymal transition (EMT) is involved in pathological processes including fibrotic disorders and cancer invasion and metastasis. Alterations of the cell-extracellular matrix (ECM) interaction also contribute to those pathological settings. However, the functional interplay between EMT and cell-ECM interaction is poorly understood. Here, we show that tumor necrosis factor (TNF)-alpha, a potent mediator of inflammation, induces EMT-associated fibrosis in retinal pigment epithelial cells, and that this is regulated by hyaluronan (HA)-CD44-Moesin interaction. TNF-alpha elicits both HA synthesis and Moesin phosphorylation through protein kinase C activation, promoting binding of CD44 to the newly synthesized HA. The HA-CD44-Moesin interaction leads to cell-cell dissociation through actin remodeling and increased cellular motility associated with mesenchymal phenotype. Furthermore, we established an in vivo model of TNF-alpha-induced fibrosis in the mouse eye, and the ocular fibrosis was completely suppressed in CD44-null mice. Therefore, HA production and its interaction with CD44 plays essential role in TNF-alpha-induced-EMT, and the interference of the complex formation can be a new strategy for the fibrotic disorders. ARPE19 cell lines were treated with TGF and TNF for 6 and 42 hour. Each experiment were repeated three times. But 1hour experiment was repeated two times. For this submission, total RNA was extracted from TGF- or TNF-treated ARPE-19 cells and differential gene expression between each time point (6 and 42 hours) was determined using genechip arrays (Affymetrix, Human Genome U133).

2010-03-23 | E-GEOD-15205 | biostudies-arrayexpress

Transcription profiling of Caco-2 and T84 human cell lines treated with flagellin, lymphotox beta or TNF alpha

Project description:14 day old Caco-2 and T84 cells were treated for 4 hours with flagellin, lymphotox beta or TNF alpha, respectively, and their expression profile compared to non-stimulated cells.

2007-08-04 | E-GEOD-1474 | biostudies-arrayexpress

Caco-2 and T84 cells stimulated with with flagellin, lymphotox beta or TNF alpha

Project description:14 day old Caco-2 and T84 cells were treated with flagellin, lymphotox beta or TNF alpha, respectively, and their expression profile compared to non-stimulated cells. Keywords: other

2004-06-16 | GSE1474 | GEO

NMuMG cell response to TGF-beta and TGF-beta +2APB treatments

Project description:Recent studies demonstrate that Ca2+ signaling has an important role in EMT. Use of Ca2+ blockers such as 2APB can inhibit cell migration induced by TGF-β. Interestingly, we see an unexpected increase in Snail expression upon Ca2+ blocker treatment of both MCF10A and NMuMG cells; this increase is not observed with 2APB treatment alone. Therefore, we believe that 2APB plays a synergistic role with TGF-β in Snail induction. We propose to investigate the gene networks that change following 2APB +TGF-β treatment.

2018-07-31 | GSE98596 | GEO

Transcriptional effects of TNF-α and TGF-β1 on human umbilical vein endothelial cells

2012-10-31 | GSE33416 | GEO

Effect of overexpression and depletion of MCEMP1 following stimulation of THP1 cells with TGF-beta

Project description:Effect of overexpression and depletion of MCEMP1 following stimulation of THP1 cells with TGF-beta

2023-11-13 | GSE247270 | GEO

Mice VSMCs: Control vs. TNF-α cultured

Project description:Transcriptional profiling of mouse VSMCs comparing control with VSMCs cultured with TNF-α Apoptosis of vascular smooth muscle cells (VSMCs) is a process that regulates vessel remodeling in various cardiovascular diseases. The specific mechanisms that control VSMC apoptosis remain unclear. The present study aimed to investigate whether microRNA-494 (miR-494) is involved in regulating VSMC apoptosis and its underlying mechanisms. Cell death ELISA and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assays were used to detect apoptosis of murine VSMCs following stimulation with tumor necrosis factor(TNF-α). The results indicated that TNF-α-upregulated VSMC apoptosis in a dose-dependent manner. Microarray analysis was used to evaluate the expression profile of microRNAs following TNF-α-stimulation in murine VSMCs. The expression of miR-494 was downregulated, whereas B-cell lymphoma 2-like 11 (BCL2L11) protein expression levels were upregulated in VSMCs following treatment with TNF- . Luciferase reporter assays confirmed that BCL2L11 was a direct target of miR-494. Transfection with miR-494 mimics decreased VSMC apoptosis and downregulated BCL2L11 protein levels. Conversely, transfection with miR-494 inhibitors increased cell apoptosis and upregulated BCL2L11 protein levels, suggesting that miR-494 may function as an essential regulator of BCL2L11. The increase in apoptosis caused by miR-494 inhibitors was abolished in cells co-transfected with BCL2L11-targeting small interfering RNA. The findings of the present study revealed that miR-494 inhibited TNF-α-induced VSMC apoptosis by downregulating the expression of BCL2L11.

2019-02-28 | GSE127016 | GEO

Differential protein secretome induced by TNF-alpha

Project description:Endothelial-mesenchymal-transition (EndMT) is an important source of cancer-associated fibroblasts (CAFs), which are known to facilitate tumor progression. We have previously shown that EndMT is present in pancreatic tumors and that deficiency of the Tie1 receptor induces EndMT in human endothelial cells. Pancreatic tumors are characterized by the presence of tumor necrosis factor-α (TNF-α). We now show that TNF-α strongly induces human endothelial cells to undergo EndMT. In order to know the secretory feature of cells which undergo EndMT by TNF-α, we conducted a comparative analysis of HMVEC secretome treated or not for 24h and 48h with TNF-α. Secretome study shows that cells treated with TNF-α have an important fibroblast-like secretory capacity, and a proinflamatory signature. Moreover, Ingenuity Pathway Analysis (IPA) shows that pathways implicated in migration, inflammation and fibrosis are predicted to be activated and that necrosis and apoptosis pathways are inhibited. Accordingly cell survival, viability and cycle progression are activated. We show that TNF-α- treated cells secrete proteins related to 16 protumoral pathways, confirming their fibroblastic characteristic. Finally, among the predicted upstream regulators activated, IPA analysis shows that, TNFSF12 and its receptor are present at hight levels in PDAC patients. Altogether these results show the fibroblastic characteristic of treated cells and demonstrate that TNF-α induces CAFs.

2021-09-08 | PXD014488 | 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