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Integrated multi-omics characterization reveals metabolic reprogramming associated with impaired mitochondrial function in clear cell renal cell carcinoma.

ABSTRACT: Integrated multi-omics characterization reveals metabolic reprogramming associated with impaired mitochondrial function in clear cell renal cell carcinoma.

PROVIDER: PRJNA483492 | ENA |

REPOSITORIES: ENA

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Integrated multi-omics characterization reveals metabolic reprogramming associated with impaired mitochondrial function in clear cell renal cell carcinoma.

Project description:An altered metabolism is involved in the development of clear cell - renal cell carcinoma (ccRCC), and in this tumor many altered genes play a fundamental role in controlling cell metabolic activities. In this study we delineated a large-scale metabolomic profile of human ccRCC, and integrated it with transcriptomic data to connect the variations in cancer metabolism with gene expression changes. Moreover, to better analyze the specific contribution of metabolic gene alterations potentially associated with tumorigenesis and tumor progression, we evaluated the transcription profile of primary renal tumor cells. Untargeted metabolomic analysis revealed a signature of an increased glucose uptake and utilization in ccRCC. In addition, metabolites related to pentose phosphate pathway were also altered in the tumor samples in association with changes in Krebs cycle intermediates and related metabolites. Using an integrated multi-omics approach we identified NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 4-like 2 (NDUFA4L2) as the most highly expressed gene in renal cancer cells and evaluated its role in sustaining angiogenesis, chemoresistance, and mitochondrial dysfunction. Finally we showed that silencing of NDUFA4L2 affects cell viability, increases mitochondrial mass, and induces ROS generation in hypoxia. These findings delineate a ccRCC metabolic signature characterized by an anaerobic switch that favors rerouting of the sugar metabolism toward the PPP, and impairs the mitochondrial activity though the overexpression of NDUFA4L2. Thus, this protein could serve as a marker of ccRCC aggressiveness, as well as a potential novel therapeutic target.

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