J Mol Med (2017) 95:951–963 DOI 10.1007/s00109-017-1552-2 ORIGINAL ARTICLE The KISS1 metastasis suppressor appears to reverse the Warburg effect by shifting from glycolysis to mitochondrial beta-oxidation 1 1,2 1,3 Sharon J. Manley & Wen Liu & Danny R. Welch Received: 1 March 2017 /Revised: 15 May 2017 /Accepted: 23 May 2017 /Published online: 8 June 2017 Springer-Verlag Berlin Heidelberg 2017 . . . Abstract Keywords KISS1 Metastasis Lipid metabolism The shift by cancer cells toward aerobic glycolysis (Warburg Glycolysis effect) confers selective advantages by utilizing nutrients (e.g., lipids, amino acids, and nucleotides) to build biomass. Lipogenesis is generally enhanced, and its inhibition diminishes proliferation and survival. Re-expression of the metastasis sup- Introduction pressor KISS1 in human melanoma cells results in greater mito- chondrial biogenesis, inhibition of glycolysis, utilization of beta- Metabolic reprogramming has long been recognized as a bio- oxidation to provide energy, elevated oxidation of exogenous chemical change in cancer cells. Otto Warburg described how fatty acids, and increased expression of early-phase lipogenesis cancer cells grown under normoxic conditions utilize aerobic genes at both mRNA and protein levels. Correspondingly, the glycolysis, resulting in increased glucose uptake and lactic energy sensor AMPKβ is phosphorylated, resulting in inhibitory acid production
Journal of Molecular Medicine – Springer Journals
Published: Jun 8, 2017
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