Journal
CANCERS
Volume 12, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/cancers12071814
Keywords
prostate cancer; metabolomics; urea cycle; fumarate; oncometabolite; NF kappa B
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Funding
- German Federal Ministry of Education and Research (BMBF)
- National Natural Science Foundation of China [21876169, 21874130, 21934006]
- National Key Research and Development Program of China [2017YFC0906900]
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Despite it being the most common incident of cancer among men, the pathophysiological mechanisms contributing to prostate cancer (PCa) are still poorly understood. Altered mitochondrial metabolism is postulated to play a role in the development of PCa. To determine the key metabolites (which included mitochondrial oncometabolites), benign prostatic and cancer tissues of patients with PCa were analyzed using capillary electrophoresis and liquid chromatography coupled with mass spectrometry. Gene expression was studied using real-time PCR. In PCa tissues, we found reduced levels of early tricarboxylic acid cycle metabolites, whereas the contents of urea cycle metabolites including aspartate, argininosuccinate, arginine, proline, and the oncometabolite fumarate were higher than that in benign controls. Fumarate content correlated positively with the gene expression of oncogenic HIF1 alpha and NF kappa B pathways, which were significantly higher in the PCa samples than in the benign controls. Furthermore, data from the TCGA database demonstrated that prostate cancer patients with activated NF kappa B pathway had a lower survival rate. In summary, our data showed that fumarate content was positively associated with carcinogenic genes.
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