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

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

PROVIDER: PRJNA714902 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13977900.fastq.gz	Fastqsanger.gz
	SRR13977901.fastq.gz	Fastqsanger.gz
	SRR13977902.fastq.gz	Fastqsanger.gz
	SRR13977903.fastq.gz	Fastqsanger.gz
	SRR13977904.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

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

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

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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

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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.

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

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