Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Polyunsaturated Fatty Acids from Astrocytes Activates PPAR Gamma Signaling in Cancer Cells to Promote Brain Metastasis

ABSTRACT: Polyunsaturated Fatty Acids from Astrocytes Activates PPAR Gamma Signaling in Cancer Cells to Promote Brain Metastasis

PROVIDER: PRJNA566243 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10142800.fastq.gz	Fastqsanger.gz
	SRR10142801.fastq.gz	Fastqsanger.gz
	SRR10142802.fastq.gz	Fastqsanger.gz
	SRR10142803.fastq.gz	Fastqsanger.gz
	SRR10142804.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Polyunsaturated Fatty Acids from Astrocytes Activates PPAR Gamma Signaling in Cancer Cells to Promote Brain Metastasis

Project description:Brain metastasis, the most ominous form of melanoma and carcinoma, is the consequence of favorable interactions between the invaded cancer cells and the brain cells. Peroxisome proliferator-activated receptor gamma (PPARɣ) has ambiguous functions in cancer development and its relevance in advanced brain metastasis remains unclear. Here, we demonstrate that astrocytes, the unique brain glia cells, activate PPARɣ in brain metastatic cancer cells. PPARɣ activation enhances cell proliferation and metastatic outgrowth in the brain. Mechanistically, astrocytes have a high content of polyunsaturated fatty acids that acts as ‘donors’ of PPARɣ activators to the invaded cancer cells. In clinical samples, PPARɣ signaling is significantly higher in brain metastatic lesions. Notably, systemic administration of PPARɣ antagonist significantly reduces brain metastatic burden in vivo. Our study clarifies a prometastatic role for PPARɣ signaling in cancer metastasis in the lipid rich brain microenvironment and argues for the use of PPARɣ blockade to treat brain metastasis.

2020-09-17 | GSE137687 | GEO

Neuronal polyunsaturated fatty acids are protective in FTD/ALS

Project description:Neuronal polyunsaturated fatty acids are protective in FTD/ALS

| PRJNA1073517 | ENA

Microenvironmental arginine restriction sensitizes pancreatic cancers to polyunsaturated fatty acids by suppression of lipid synthesis

Project description:Nutrient limitation in the microenvironment of poorly perfused tumors constrains the metabolism of cancer cells. Identifying these microenvironmental constraints can provide new insight into the nutritional biochemistry of tumors and reveal metabolic liabilities of cancer cells. We have found that limitation of arginine in pancreatic cancers inhibits fatty acid synthesis by suppressing the lipogenic transcription factor SREBP1. SREBP1-driven fatty acid synthesis produces saturated and monounsaturated fatty acids. Producing these fatty acids enables cells to maintain a balance of differently saturated fatty acids needed for lipid homeostasis, even upon exposure to environments enriched in one specific class of fatty acids. Given the constraints on lipid synthesis in the microenvironment, we asked if pancreatic cancers are sensitive to exposure to fats with imbalanced levels of saturated and unsaturated fats. We found microenvironmental constraints on lipid synthesis sensitize pancreatic cancer cells and tumors to exposure to fat sources that are enriched in polyunsaturated fatty acids. Thus, amino acid restriction in the tumor microenvironment constrains lipid metabolism in pancreatic cancer, which renders pancreatic tumors incapable of maintaining lipid homeostasis upon exposure to polyunsaturated-enriched fats.

2025-02-11 | GSE288530 | GEO

The consequences of n-3 polyunsaturated fatty acids (PUFA) depletion on hepatic lipid metabolism in mice

Project description:In the present study, we investigated the consequences of n-3 polyunsaturated fatty acids (PUFA) depletion on hepatic lipid metabolism in mice fed during three months with a diet presenting a high n-6/n-3 PUFA ratio to induce n-3 PUFA depletion. Microarray analyses were performed to identify the molecular targets involved in the development of hepatic steatosis associated with n-3 PUFA depletion.

2011-08-26 | GSE26986 | GEO

Neuronal polyunsaturated fatty acids are protective in FTD/ALS

Project description:We report a conserved transcriptomic signature of reduced fatty acid and lipid metabolism gene expression in human post-mortem ALS spinal cord and a Drosophila model of the most common genetic cause of FTD/ALS, a repeat expansion in C9orf72. To investigate lipid alterations, we performed lipidomics on C9FTD/ALS iPSC-neurons and post-mortem FTLD brain tissue. This revealed a common and specific reduction in phospholipid species containing polyunsaturated fatty acids (PUFAs). To determine whether this PUFA deficit contributes to neurodegeneration, we fed C9FTD/ALS flies PUFAs, which yielded a modest increase in survival. However, increasing PUFA levels specifically in neurons of the C9orf72 flies, by overexpressing fatty acid desaturase enzymes, led to a substantial extension of lifespan. Neuronal overexpression of fatty acid desaturases also suppressed stressor induced neuronal death in C9FTD/ALS patient iPSC-neurons. These data implicate neuronal fatty acid saturation in the pathogenesis of FTD/ALS and suggest that interventions to increase PUFA levels specifically within neurons will be beneficial.

2024-11-15 | GSE255099 | GEO

Transcriptomic response to variation in habitual n-3 polyunsaturated fatty acid intake

Project description:Analysis of variation in subcutaneous adipose tissue gene expression in response to dietary intake of n-3 polyunsaturated fatty acids, as assessed in a cohot of individuals with metabolic syndrome. Outcomes from this study provide insight on molecular details of dietary effects on gene expression and metabolic health. Subcutaneous adipose tissue samples were taken from a cohort of seventeen individuals with metabolic syndrome. Habitual intake of n-3 polyunsaturated fatty acids was assessed with 3-day weighed food journals.

2011-08-31 | E-GEOD-28070 | biostudies-arrayexpress

The Ability of Dietary Polyunsaturated Fatty Acids to Protect Against Liver Inflammation and Non-Alcoholic Steatohepatitis (NASH) is Dependent on Gut Microbes

Project description:The Ability of Dietary Polyunsaturated Fatty Acids to Protect Against Liver Inflammation and Non-Alcoholic Steatohepatitis (NASH) is Dependent on Gut Microbes

2025-10-02 | PXD068318 | Pride

The roles of ppar-delta and ppar-gamma in regulating the metabolic switch between oxidation and storage of fats in white adipose tissue

Project description:Obesity is a major risk factor for the development of insulin resistance and type II diabetes. The nuclear receptors PPAR-delta and PPAR-gamma play a central role in regulating metabolism in adipose tissue, as well as being targets for the treatment of insulin resistance. The metabolic effects of PPAR-delta and PPAR-gamma activation have been examined both in vivo in white adipose tissue from ob/ob mice and in vitro in cultured 3T3-L1 adipocytes using a combined 1H NMR spectroscopy and mass spectrometry metabolomic methodology to understand the contrasting roles of these receptors. These steady state measurements were supplemented with 13C-stable isotope substrate labeling to assess fluxes, respirometry and transcriptomic microarray analysis. The metabolic effects of the two receptors were readily distinguished, with PPAR-gamma activation characterised by increased fat storage and fat synthesis/elongation, while activation of PPAR-delta caused increased fatty acid beta-oxidation, TCA cycle rate and oxidation of extracellular branch chain amino acids. Stimulated glycolysis and increased desaturation of fatty acids were the only common pathways. PPAR-delta has a role as an anti-obesity target as well as an anti-diabetic.

2011-07-14 | GSE26207 | GEO

DEHP activation of PPAR(alpha) and CAR regulartory pathway in mouse liver

Project description:Characterization of Peroxisome Proliferator-Activated Receptor alpha (PPAR(alpha)) - Independent Effects of PPAR(alpha) Activators in the Rodent Liver: Di-(2-ethylhexyl) phthalate Activates the Constitutive Activated Receptor data files in this series indicate the involvement of PPAR(alpha) and CAR regulatory pathway after DEHP treatment. Keywords: gene expression/microarray

2009-10-20 | GSE18564 | GEO

Induction of lipid oxidation gene expression by polyunsaturated fatty acids of marine origin in small intestine of mice

Project description:Dietary polyunsaturated fatty acids (PUFA) act as potent natural hypolipidemics and are linked to many health benefits in humans and in animal models. Mice fed long-term a high fat diet, in which medium-chain alpha linoleic acid (ALA) was partially replaced by long-chain docosahexaenoic (DHA) and eicosapentaenoic (EPA) fatty acids, showed reduced accumulation of body fat and prevention of insulin resistance, besides increased mitochondrial beta-oxidation in white adipose tissue and decreased plasma lipids. ALA, EPA and DHA all belong to PUFA of n-3 series. The intestine is a gatekeeper organ for ingested lipids. To examine the potential contribution of the intestine in the beneficial effects of EPA and DHA, this study assessed gene expression changes using whole genome microarray analysis on small intestinal scrapings. The main biological process affected was lipid metabolism. Fatty acid uptake, peroxisomal and mitochondrial beta-oxidation, and omega-oxidation of fatty acids were all increased. Quantitative real time PCR and intestinal fatty acid oxidation measurements ([14C(U)]-palmitate) confirmed significant gene expression differences in a dose-dependent manner. Furthermore, no major changes in the expression of lipid metabolism genes were observed in colonic scrapings. In conclusion, we show that marine n-3 fatty acids regulate small intestinal gene expression patterns. Since this organ contributes significantly to whole organism energy use, this adaptation of the small intestine may contribute to the complex and observed beneficial physiological effects of these natural compounds under conditions that will normally lead to development of obesity and diabetes.

2009-04-01 | GSE11936 | 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