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Lack of electron acceptors contributes to redox stress and growth arrest in asparagine-starved sarcoma cells

ABSTRACT: Lack of electron acceptors contributes to redox stress and growth arrest in asparagine-starved sarcoma cells

PROVIDER: PRJNA644660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12170001_1.fastq.gz	Fastqsanger.gz
	SRR12170001_2.fastq.gz	Fastqsanger.gz
	SRR12170002_1.fastq.gz	Fastqsanger.gz
	SRR12170002_2.fastq.gz	Fastqsanger.gz
	SRR12170003_1.fastq.gz	Fastqsanger.gz

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Lack of electron acceptors contributes to redox stress and growth arrest in asparagine-starved sarcoma cells

Project description:Adequate availability of the non-essential amino acid asparagine is necessary to support growth and survival of sarcoma cells. The three top pathways enriched among transcripts upregulated in asparagine-depleted cells included ribosome, aminoacyl tRNA biosynthesis and oxidative phosphorylation.

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Lack of Electron Acceptors Contributes to Redox Stress and Growth Arrest in Asparagine-Starved Sarcoma Cells.

Project description:Amino acids are integral components of cancer metabolism. The non-essential amino acid asparagine supports the growth and survival of various cancer cell types. Here, different mass spectrometry approaches were employed to identify lower aspartate levels, higher aspartate/glutamine ratios and lower tricarboxylic acid (TCA) cycle metabolite levels in asparagine-deprived sarcoma cells. Reduced nicotinamide adenine dinucleotide (NAD+)/nicotinamide adenine dinucleotide hydride (NADH) ratios were consistent with redirection of TCA cycle flux and relative electron acceptor deficiency. Elevated lactate/pyruvate ratios may be due to compensatory NAD+ regeneration through increased pyruvate to lactate conversion by lactate dehydrogenase. Supplementation with exogenous pyruvate, which serves as an electron acceptor, restored aspartate levels, NAD+/NADH ratios, lactate/pyruvate ratios and cell growth in asparagine-deprived cells. Chemicals disrupting NAD+ regeneration in the electron transport chain further enhanced the anti-proliferative and pro-apoptotic effects of asparagine depletion. We speculate that reductive stress may be a major contributor to the growth arrest observed in asparagine-starved cells.

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