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Tumor reliance on cytosolic versus mitochondrial one-carbon flux depends on folate availability

ABSTRACT: Tumor reliance on cytosolic versus mitochondrial one-carbon flux depends on folate availability

PROVIDER: PRJNA641374 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12073485.fastq.gz	Fastqsanger.gz
	SRR12073486.fastq.gz	Fastqsanger.gz
	SRR12073487.fastq.gz	Fastqsanger.gz
	SRR12073488.fastq.gz	Fastqsanger.gz
	SRR12073489.fastq.gz	Fastqsanger.gz

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Tumor reliance on cytosolic versus mitochondrial one-carbon flux depends on folate availability

Project description:The goal of this analysis is to detect the differentially expressed genes between cells cultured in high or low folate condition.

2020-06-24 | GSE153023 | GEO

Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency [RNA-seq]

Project description:we report that U251 glioblastoma tumor spheres exhibit low cytosolic folate cycle and a reprogrammmed mitochondrial folate cycle that is presumably oriented towards oxidizing the formyl group to CO2 with the production of TetraHydroFolate and release of NADPH instead of synthesizing formate

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Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency [methylation]

Project description:What is known is that methionine-dependency is a feature of some cancers. So far, it was attributed to mutations in genes involved in the methionine de novo or salvage pathways. What is new is that in this work we propose that methionine dependency stems from an altered cellular metabolism. We provide evidence that in U251 glioblastoma cell line, only cancer stem cells -isolated as tumor spheres in non adherent conditions- are methionine dependent and not monolayer cells grown in adherent conditions. Transcriptome wide-sequencing reveals that several genes involved in cytosolic folate cycle are downregulated whereas some transcripts of genes involved in mitochondrial folate cycle are upregulated. Genome wide DNA methylation does not account for these changes in gene expression. Mass spectrometry measurements confirm that tumor spheres display low cytosolic folate cycle unable to produce enough 5-methyltetrahydrofolate to remethylate homocystein to methionine. This decreased 5-methyltetrahydrofolate bioavailability is presumably due to a reprogrammed mitochondrial folate cycle which instead of synthesizing formate, intended to fuel the cytosolic folate cycle, oxidizes the formyl group to CO2 with the attendant reduction of NADP+ to NADPH and release of tetrahydrofolate. The originality of this work resides in that it replaces methionine deprivation as a useful nutritional strategy in cancer growth control since cancer stem cells are much more tumoregenic than their non stem-like counterparts. Second, it reveals that the primary default responsible of the reprogrammation of folate metabolism originates in the mitochondria. Thus, mitochondrial enzymes could be novel and more promising anticancer targets than dihydrofolate reductase (DHFR), the current target of drug therapy linked with folate metabolism.

2019-07-01 | GSE117448 | GEO

Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency

Project description:Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency

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Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency [methylation]

Project description:Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency [methylation]

| PRJNA482423 | ENA

Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency [RNA-seq]

Project description:Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency [RNA-seq]

| PRJNA482432 | ENA

Reversal of Cytosolic One-Carbon Flux Compensates for Loss of the Mitochondrial Folate Pathway.

Project description:One-carbon (1C) units for purine and thymidine synthesis can be generated from serine by cytosolic or mitochondrial folate metabolism. The mitochondrial 1C pathway is consistently overexpressed in cancer. Here, we show that most but not all proliferating mammalian cell lines use the mitochondrial pathway as the default for making 1C units. Clustered regularly interspaced short palindromic repeats (CRISPR)-mediated mitochondrial pathway knockout activates cytosolic 1C-unit production. This reversal in cytosolic flux is triggered by depletion of a single metabolite, 10-formyl-tetrahydrofolate (10-formyl-THF), and enables rapid cell growth in nutrient-replete conditions. Loss of the mitochondrial pathway, however, renders cells dependent on extracellular serine to make 1C units and on extracellular glycine to make glutathione. HCT-116 colon cancer xenografts lacking mitochondrial 1C pathway activity generate the 1C units required for growth by cytosolic serine catabolism. Loss of both pathways precludes xenograft formation. Thus, either mitochondrial or cytosolic 1C metabolism can support tumorigenesis, with the mitochondrial pathway required in nutrient-poor conditions.

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Dietary folate limitation late in life

Project description:Folate is a vitamin essential for cell growth and has been used to prevent congenital abnormalities. However, little is known about how folate affects health in older adults. We examined healthspan as a function of dietary folate intake. To begin to measure such effects, we performed a small (2x2; sex-by-diet) pilot study in the long-lived inbred mouse strain C57BL/6.

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Project description:This SuperSeries is composed of the following subset Series: GSE9242: Dietary folate depletion and repletion in A/J and C57BL/6J mice GSE9243: Dietary folate depletion and repletion in C57BL/6J mice, ApoE knockout mice, and choline supplemented C57BL/6J mice Keywords: SuperSeries Refer to individual Series

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Gene expression alteration in human fibroblast cells after folate depletion

Project description:The molecular basis linking folate deficiency to certain health conditions and developmental defects is complex and not fully understood. In this study, we examined the consequences of folate deficiency on global gene expression by microarray analysis and compared transcript levels in normal human fibroblast cells (GM03349) grown in folate deficient and sufficient medium. Keywords: folate depletion, stress response, comparative genomic hybridization

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