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Homo sapiens

ABSTRACT: Whole exome sequencing of renal oncocytoma samples

PROVIDER: PRJNA387033 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5574310_1.fastq.gz	Fastqsanger.gz
	SRR5574310_2.fastq.gz	Fastqsanger.gz
	SRR5574311_1.fastq.gz	Fastqsanger.gz
	SRR5574311_2.fastq.gz	Fastqsanger.gz
	SRR5574312_1.fastq.gz	Fastqsanger.gz

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Project description:Renal oncocytomas are rare benign tumors of the kidney and are characterized by a deficient complex I (CI) enzyme activity of the oxidative phosphorylation (OXPHOS) system caused by mitochondrial DNA (mtDNA) mutations. Yet, little is known about the underlying molecular mechanisms and alterations of metabolic pathways in this tumor. We compared renal oncocytomas with adjacent matched normal kidney tissues on a global scale by multi-omics approaches, including whole exome sequencing (WES), proteomics, metabolomics, and metabolic pathway simulation. The abundance of proteins localized to mitochondria increased more than 2-fold, the only exception was a strong decrease in the abundance for CI subunits that revealed multiple pathogenic heteroplasmic mtDNA mutations by WES. We also observed renal oncocytomas to dysregulate main metabolic pathways, shunting away from gluconeogenesis and lipid metabolism. Nevertheless, the abundance of energy carrier molecules such as of NAD+, NADH, NADP, ATP and ADP were significantly higher in renal oncocytoma. Finally, a tremendous 5000-fold increase of the reactive oxygen species (ROS) scavenger glutathione (GSH) can be regarded as a new hallmark of renal oncocytoma. Our findings demonstrate that renal oncocytomas undergo a metabolic switch to eliminate ATP consuming processes to ensure a sufficient energy supply for the tumor.

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