Loss of succinate dehydrogenase activity results in dependency on pyruvate carboxylation for cellular anabolism View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-11-02

AUTHORS

Charlotte Lussey-Lepoutre, Kate E. R. Hollinshead, Christian Ludwig, Mélanie Menara, Aurélie Morin, Luis-Jaime Castro-Vega, Seth J. Parker, Maxime Janin, Cosimo Martinelli, Chris Ottolenghi, Christian Metallo, Anne-Paule Gimenez-Roqueplo, Judith Favier, Daniel A. Tennant

ABSTRACT

The tricarboxylic acid (TCA) cycle is a central metabolic pathway responsible for supplying reducing potential for oxidative phosphorylation and anabolic substrates for cell growth, repair and proliferation. As such it thought to be essential for cell proliferation and tissue homeostasis. However, since the initial report of an inactivating mutation in the TCA cycle enzyme complex, succinate dehydrogenase (SDH) in paraganglioma (PGL), it has become clear that some cells and tissues are not only able to survive with a truncated TCA cycle, but that they are also able of supporting proliferative phenotype observed in tumours. Here, we show that loss of SDH activity leads to changes in the metabolism of non-essential amino acids. In particular, we demonstrate that pyruvate carboxylase is essential to re-supply the depleted pool of aspartate in SDH-deficient cells. Our results demonstrate that the loss of SDH reduces the metabolic plasticity of cells, suggesting vulnerabilities that can be targeted therapeutically. More... »

PAGES

8784

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms9784

DOI

http://dx.doi.org/10.1038/ncomms9784

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044755286

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26522426


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