Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells II

ABSTRACT: Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells II

PROVIDER: PRJNA714908 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13977848.fastq.gz	Fastqsanger.gz
	SRR13977849.fastq.gz	Fastqsanger.gz
	SRR13977850.fastq.gz	Fastqsanger.gz
	SRR13977851.fastq.gz	Fastqsanger.gz
	SRR13977852.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells II

Project description:Chronic inflammation promotes cancer progression by affecting the tumor cells and their microenvironment. Here, we demonstrate that the continuous stimulation (6 weeks) of triple-negative breast tumor cells (TNBC) by the potent pro-inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β) had a robust effect on gene expression, demonstrating that the cancer cells have been skewed to strong pro-inflammatory phenotype. Moreover, continuous TNFα + IL-1β stimulation has reduced cell-to-cell contacts in the cancer cells and has induced metabolic plasticity in TNBC cells: this was exemplified by increase in active mitochondria area and elevations in the glycolytic as well as mitochondrial respiratory potential of the cancer cells (OXPHOS). Glycolysis has induced p65 activation and has led to increased transcription and expression of pro-metastatic chemokines such as CXCL8, CXCL1 and CCL2 and sICAM-1; agreeing with the ability of these chemokines to induce the recruitment of deleterious myeloid cells to tumors, mainly inhibition of glycolysis has given rise to reduced monocytic cell migration, in vitro and in vivo, in response to cancer cell supernatants obtained following continuous TNFα + IL-1β stimulation. Such inflammation-induced metabolic plasticity, which promotes metastatic cascades in TNBC, may have important clinical implications in the treatment of TNBC patients

2021-05-30 | GSE169017 | GEO

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells I

2021-05-30 | GSE169016 | GEO

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells

Project description:Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells

| PRJNA714902 | ENA

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells I

Project description:Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells I

| PRJNA714905 | ENA

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-30 | GSE169018 | GEO

Continuous Inflammatory Stimulation Leads via Metabolic Plasticity to a Prometastatic Phenotype in Triple-Negative Breast Cancer Cells.

Project description:Chronic inflammation promotes cancer progression by affecting the tumor cells and their microenvironment. Here, we demonstrate that a continuous stimulation (~6 weeks) of triple-negative breast tumor cells (TNBC) by the proinflammatory cytokines tumor necrosis factor α (TNFα) + interleukin 1β (IL-1β) changed the expression of hundreds of genes, skewing the cells towards a proinflammatory phenotype. While not affecting stemness, the continuous TNFα + IL-1β stimulation has increased tumor cell dispersion and has induced a hybrid metabolic phenotype in TNBC cells; this phenotype was indicated by a transcription-independent elevation in glycolytic activity and by increased mitochondrial respiratory potential (OXPHOS) of TNBC cells, accompanied by elevated transcription of mitochondria-encoded OXPHOS genes and of active mitochondria area. The continuous TNFα + IL-1β stimulation has promoted in a glycolysis-dependent manner the activation of p65 (NF-kB), and the transcription and protein expression of the prometastatic and proinflammatory mediators sICAM-1, CCL2, CXCL8 and CXCL1. Moreover, when TNBC cells were stimulated continuously by TNFα + IL-1β in the presence of a glycolysis inhibitor, their conditioned media had reduced ability to recruit monocytes and neutrophils in vivo. Such inflammation-induced metabolic plasticity, which promotes prometastatic cascades in TNBC, may have important clinical implications in treatment of TNBC patients.

| S-EPMC8229065 | biostudies-literature

Retrotransposon derepression leads to activation of the unfolded protein response and apoptosis in pro B cells

Project description:The establishment of distinct transcription programs during development is controlled by transcription factor networks acting in specific chromatin environments. The H3K9me3-specific histone methyltransferase Setdb1 impacts on transcriptional regulation by repressing both developmental genes and retrotransposons. How impaired retrotransposon silencing may lead to developmental phenotypes is currently unclear. Here we show that loss of Setdb1 in pro-B cells completely abrogates B cell development. In pro-B cells, Setdb1 is dispensable for silencing of lineage-inappropriate developmental genes. Instead, we detect strong derepression of endogenous Murine Leukemia Virus (MLV) copies. Production of MLV proteins leads to activation of the unfolded protein response pathway and apoptosis. Thus, our data demonstrate that B cell development critically depends on the proper repression of retrotransposon sequences through Setdb1. Transcriptomic and chromatin analysis of control and Setdb1-deficient pro-B cells

2016-07-20 | E-GEOD-77636 | biostudies-arrayexpress

Deoxyhypusine Synthase Promotes a Pro-Inflammatory Macrophage Phenotype

Project description:Deoxyhypusine Synthase Promotes a Pro-Inflammatory Macrophage Phenotype

| PRJNA604198 | ENA

Retrotransposon derepression leads to activation of the unfolded protein response and apoptosis in pro B cells

2016-07-20 | GSE77636 | GEO

Machine learning inference of continuous single-cell state transitions during myoblast differentiation and fusion

Project description:Cells dynamically change their internal organization via continuous cell state transitions to mediate a plethora of physiological processes. Understanding such continuous processes is severely limited due to a lack of tools to measure the holistic physiological state of single cells undergoing a transition. We combined live-cell imaging and machine learning to quantitatively monitor skeletal muscle precursor cell (myoblast) differentiation during multinucleated muscle fiber formation. Our machine learning model predicted the continuous differentiation state of single primary murine myoblasts over time and revealed that inhibiting ERK1/2 leads to a gradual transition from an undifferentiated to a terminally differentiated state 7.5-14.5 hours post inhibition. Myoblast fusion occurred ~3 hours after predicted terminal differentiation. Moreover, we showed that our model could predict that cells have reached terminal differentiation under conditions where fusion was stalled, demonstrating potential applications in screening. This method can be adapted to other biological processes to reveal connections between the dynamic single-cell state and virtually any other functional readout.

2024-05-23 | PXD047198 | 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