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- W2936997567 abstract "In a recent review, Zhanyu Wang and Chenfang Dong [ 1 Wang Z. Dong C. Gluconeogenesis in cancer: function and regulation of PEPCK, FBPase, and G6Pase. Trends Cancer. 2019; 5: 30-45 Abstract Full Text Full Text PDF PubMed Scopus (104) Google Scholar ] underlined the fact that cancer cells may engage gluconeogenesis to support their anabolic biosynthesis, a pathway supported by noncarbohydrate precursors and regulated by three enzymes: PEPCK, FBPase, and G6Pase. Reviewing the functions of FBPase, the authors explained that it suppresses HIF-1 α activity and, thus, transcription of HIF-1α target genes, in particular PDK1. The inactivation of FBPase triggers a switch from glycolysis to oxidative phosphorylation (OXPHOS), which participates in the tumor-suppressing effects of FBPase. Regarding processes inhibiting FBP1 in many cancers and leading to a truncated gluconeogenesis supporting biosynthesis, the authors emphasized the role of epigenetic dysregulation (methylation and acetylation) of the FBP1 gene, and the action of fructose-2,6-bisphosphate (F2,6BP). This molecule produced by PFKFB (also called PFK2), in particular the PFKFB3 isoform, is an inhibitor of FBPase [ 2 Yalcin A. et al. Nuclear targeting of 6-phosphofructo-2-kinase (PFKFB3) increases proliferation via cyclin-dependent kinases. J. Biol. Chem. 2009; 284: 24223-24232 Crossref PubMed Scopus (163) Google Scholar ]. Therefore, reactivation of FBPase (directly or indirectly through PFK2 inhibition) could have anticancer effects [ 3 Nissler K. et al. Fructose 2,6-bisphosphate metabolism in Ehrlich ascites tumour cells. J. Cancer Res. Clin. Oncol. 1995; 121: 739-745 Crossref PubMed Scopus (34) Google Scholar ]." @default.
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- W2936997567 date "2019-05-01" @default.
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- W2936997567 title "Gluconeogenesis of Cancer Cells Is Disrupted by Citrate" @default.
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- W2936997567 doi "https://doi.org/10.1016/j.trecan.2019.03.002" @default.
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