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SHR Neuro Krebs Kardio Lipid

Grasmann, G; Smolle, E; Olschewski, H; Leithner, K.
Gluconeogenesis in cancer cells - Repurposing of a starvation-induced metabolic pathway?
Biochim Biophys Acta Rev Cancer. 2019; 1872(1):24-36 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Autor/innen der Med Uni Graz:
Grasmann Gabriele Agnes
Leithner Katharina
Olschewski Horst
Smolle Elisabeth
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Abstract:
Cancer cells constantly face a fluctuating nutrient supply and interference with adaptive responses might be an effective therapeutic approach. It has been discovered that in the absence of glucose, cancer cells can synthesize crucial metabolites by expressing phosphoenolpyruvate carboxykinase (PEPCK, PCK1 or PCK2) using abbreviated forms of gluconeogenesis. Gluconeogenesis, which in essence is the reverse pathway of glycolysis, uses lactate or amino acids to feed biosynthetic pathways branching from glycolysis. PCK1 and PCK2 have been shown to be critical for the growth of certain cancers. In contrast, fructose-1,6-bisphosphatase 1 (FBP1), a downstream gluconeogenesis enzyme, inhibits glycolysis and tumor growth, partly by non-enzymatic mechanisms. This review sheds light on the current knowledge of cancer cell gluconeogenesis and its role in metabolic reprogramming, cancer cell plasticity, and tumor growth. Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.

Find related publications in this database (Keywords)
Gluconeogenesis
Tumor
Metabolic plasticity
Starvation
Adaptation
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