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High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

ABSTRACT: High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

PROVIDER: PRJNA356311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5077910.fastq.gz	Fastqsanger.gz
	SRR5077990.fastq.gz	Fastqsanger.gz
	SRR5077911.fastq.gz	Fastqsanger.gz
	SRR5077912.fastq.gz	Fastqsanger.gz
	SRR5077913.fastq.gz	Fastqsanger.gz

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Similar Datasets

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program.

Project description:Systemic metabolic alterations associated with increased consumption of saturated fat and obesity are linked with increased risk of prostate cancer progression and mortality, but the molecular underpinnings of this association are poorly understood. Here, we demonstrate in a murine prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through metabolic alterations that favour histone H4K20 hypomethylation at the promoter regions of MYC regulated genes, leading to increased cellular proliferation and tumour burden. Saturated fat intake (SFI) is also associated with an enhanced MYC transcriptional signature in prostate cancer patients. The SFI-induced MYC signature independently predicts prostate cancer progression and death. Finally, switching from a high-fat to a low-fat diet, attenuates the MYC transcriptional program in mice. Our findings suggest that in primary prostate cancer, dietary SFI contributes to tumour progression by mimicking MYC over expression, setting the stage for therapeutic approaches involving changes to the diet.

| S-EPMC6761092 | biostudies-literature

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

Project description:Systemic metabolic alterations associated with increased consumption of saturated fat and obesity are linked with increased risk of prostate cancer progression and mortality but the molecular underpinnings of this association are poorly understood. Furthermore, the mechanisms by which metabolic rewiring alters the prostate cancer epigenome, the effector arm of intra- and extra-cellular signals, is equally nebulous. Here, we demonstrate, in a murine prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through metabolic alterations that favour histone H4K20 hypomethylation at the promoter regions of MYC regulated genes, leading to a HFD-dependent phenotype characterized by increased cellular proliferation and tumour burden. Importantly, these results are recapitulated in prostate cancer patients, where increased saturated fat intake (SFI), but not monounsaturated or polyunsaturated fat intake, is also associated with an enhanced MYC transcriptional signature. Additionally, the SFI-induced MYC signature independently predicts prostate cancer progression and death. Finally, a dietary intervention consisting of switching from a high-fat to control diet, greatly attenuates the MYC transcriptional program. Our findings suggest that in primary prostate cancer, dietary saturated fat intake contributes to tumour progression by mimicking MYC over expression, setting the stage for therapeutic approaches involving changes to the diet.

2019-08-21 | GSE90910 | GEO

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

Project description:Systemic metabolic alterations associated with increased consumption of saturated fat and obesity are linked with increased risk of prostate cancer progression and mortality but the molecular underpinnings of this association are poorly understood. Furthermore, the mechanisms by which metabolic rewiring alters the prostate cancer epigenome, the effector arm of intra- and extra-cellular signals, is equally nebulous. Here, we demonstrate, in a murine prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through metabolic alterations that favour histone H4K20 hypomethylation at the promoter regions of MYC regulated genes, leading to a HFD-dependent phenotype characterized by increased cellular proliferation and tumour burden. Importantly, these results are recapitulated in prostate cancer patients, where increased saturated fat intake (SFI), but not monounsaturated or polyunsaturated fat intake, is also associated with an enhanced MYC transcriptional signature. Additionally, the SFI-induced MYC signature independently predicts prostate cancer progression and death. Finally, a dietary intervention consisting of switching from a high-fat to control diet, greatly attenuates the MYC transcriptional program. Our findings suggest that in primary prostate cancer, dietary saturated fat intake contributes to tumour progression by mimicking MYC over expression, setting the stage for therapeutic approaches involving changes to the diet.

2019-08-21 | GSE90905 | GEO

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

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

2019-08-21 | GSE90912 | GEO

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

2019-08-22 | MTBLS135 | MetaboLights

Rewiring of cortical glucose metabolism fuels human brain cancer growth

Project description:Rewiring of cortical glucose metabolism fuels human brain cancer growth

| PRJNA1272587 | ENA

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Project description:High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

| PRJNA356313 | ENA

Mus musculus

Project description:High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

| PRJNA356304 | ENA

Dickkopf1 fuels inflammatory cytokine responses

Project description:Dickkopf1 fuels inflammatory cytokine responses

| PRJNA897934 | ENA

Rewiring of cortical glucose metabolism fuels human brain cancer growth

Project description:The brain avidly consumes glucose to fuel neurophysiology. Cancers of the brain, such as glioblastoma (GBM), relinquish physiological integrity and gain the ability to proliferate and invade healthy tissue. How brain cancers rewire glucose utilization to drive aggressive growth remains elusive. Here, we infused 13C-labeled glucose into patients and mice with brain cancer, coupled with quantitative metabolic flux analysis, to map the fates of glucose-derived carbon in tumor vs. cortex. Through the first direct and comprehensive measurements of carbon and nitrogen labeling in both cortex and glioma tissues, we uncover profound metabolic transformations. In human cortex, glucose carbons fuel essential physiologic processes including TCA cycle oxidation and neurotransmitter synthesis. Conversely, gliomas downregulate these processes and scavenge alternative carbon sources such as amino acids from the environment, repurposing glucose-derived carbons to generate molecules needed for proliferation and invasion. Targeting this metabolic rewiring in mice through dietary amino acid modulation selectively alters GBM metabolism, slows tumor growth, and augments the efficacy of standard-of-care treatments. These findings illuminate how aggressive brain tumors exploit glucose to suppress normal physiological activity in favor of malignant expansion and offer potential therapeutic strategies to enhance treatment outcomes.

2025-06-05 | GSE299102 | GEO

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