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To identify metabolic pathways that were perturbed in pancreatic cancer ( PC ), we investigated gene‐metabolite networks by integration of metabolomic and transcriptomic. In this research, we undertook the metabolomic study of 43 paired human  PC  samples, aiming to identify key metabolic alterations in  PC . We also carried out in vitro experiments to validate that the key metabolite cytidine and its related gene   ENTPD 8  played an important role in  PC  cell proliferation. We screened out 13 metabolites differentially expressed in PC tissue ( PCT ) by liquid chromatography/mass spectrometry analysis on 34 metabolites, and the partial least square discrimination analysis results revealed that 9 metabolites among them were remarkably altered in  PCT  compared to adjacent noncancerous tissue (variable importance in projection >1,  P  <   .05). Among the 9 metabolites, 7 might be potential biomarkers. The most significantly enriched metabolic pathway was pyrimidine metabolism. We analyzed 351 differentially expressed genes from The Cancer Genome Atlas and intersected them with Kyoto Encyclopedia of Genes and Genomes metabolic pathways. We found that   ENTPD 8  had a gene‐metabolite association with cytidine in the  CTP  dephosphorylation pathway. We verified by in vitro experiments that the  CTP  dephosphorylation pathway was changed in  PCT  compared with adjacent noncancerous tissue.   ENTPD 8  was downregulated in  PCT , causing a reduction in cytidine formation and hence weakened  CTP  dephosphorylation in pyrimidine metabolism.

Identification of ENTPD8 and cytidine in pancreatic cancer by metabolomic and transcriptomic conjoint analysis