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Frankó, A. ; Shao, Y.* ; Heni, M. ; Hennenlotter, J.* ; Hoene, M.* ; Hu, C.* ; Liu, X.* ; Zhao, X.* ; Wang, Q.* ; Birkenfeld, A.L. ; Todenhöfer, T.* ; Stenzl, A.* ; Peter, A.* ; Häring, H.-U. ; Lehmann, R. ; Xu, G.* ; Lutz, S.Z.*

Human prostate cancer is characterized by an increase in urea cycle metabolites.

Cancers 12:1814 (2020)
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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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Publication type Article: Journal article
Document type Scientific Article
Keywords Prostate Cancer ; Metabolomics ; Urea Cycle ; Fumarate ; Oncometabolite ; Nf Kappa B; Hr-mas Spectroscopy; Insulin Sensitivity; Tissue; H-1; Oncometabolites; Metabolomics; Markers; Citrate; Benign; Pseudohypoxia
Language english
Publication Year 2020
HGF-reported in Year 2020
ISSN (print) / ISBN 2072-6694
Journal Cancers
Quellenangaben Volume: 12, Issue: 7, Pages: , Article Number: 1814 Supplement: ,
Publisher MDPI
Publishing Place St Alban-anlage 66, Ch-4052 Basel, Switzerland
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes Research and Metabolic Diseases (IDM)
POF-Topic(s) 90000 - German Center for Diabetes Research
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502400-001
DOI 10.3390/cancers12071814
WOS ID WOS:000554251900001
Scopus ID 85088881058
PubMed ID 32640711
Erfassungsdatum 2020-07-28
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