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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

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			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

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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

Synergy of chemotherapy and macrophage depletion leads to T cell memory activation and durable triple negative breast cancer regression

Project description:Chemotherapy and macrophage depletion leads to T cell memory activation and durable triple negative breast cancer regression in p53 null mouse models.

2022-06-10 | GSE173260 | GEO

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

Extracellular Nicotinamide Phosphoribosyltransferase (eNAMPT) Drives Abnormal Pericyte-Rich Vasculature in Triple-Negative Breast Cancer

Project description:Tumour angiogenesis supports malignant cells with oxygen and nutrients to promote invasion and metastasis. A number of cytokines released in situ participate in the recruitment of endothelial cells and pericytes to trigger the formation of novel blood vessels, which are often abnormal, leaky, and disorganized. Nicotinamide phosphoribosyltransferase is a key intracellular enzyme involved in NAD metabolism and is up regulated in many cancers to meet bioenergetic demands. Yet, the same protein is also secreted extracellularly (eNAMPT), where it acts as a pro-inflammatory cytokine. High plasma eNAMPT levels have been reported in breast cancer patients and correlate with aggressiveness and prognosis. We now report that in a triple-negative breast cancer model, enriching the tumour microenvironment with eNAMPT leads to abundant angiogenesis and increased metastatization. Atypically, the eNAMPT-mediated pro-angiogenic effect is mainly directed to NG2+ pericytes. Indeed, eNAMPT acts as chemoattractant for pericytes and coordinates vessel-like tube formation, in synergism with the classical factor PDGF-BB. Stimulation of pericytes by eNAMPT leads to a pro-inflammatory activation, characterized by the overexpression of key chemokines (CXCL8, CXCL1, CCL2) and VCAM1, via NF-kB signalling. All these effects were ablated by the use of C269, an anti-eNAMPT neutralizing antibody, suggesting that this might represent a novel anti-angiogenic pharmacological approach for triple-negative breast cancer.

2024-10-28 | GSE277698 | GEO

OCT-2 is associated with pro-metastatic epigenomic properties of triple-negative breast cancer cells

Project description:OCT-2 is associated with pro-metastatic epigenomic properties of triple-negative breast cancer cells

| PRJNA1236320 | ENA