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From Krebs to clinic: glutamine metabolism to cancer therapy
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Journal Article
From Krebs to clinic: glutamine metabolism to cancer therapy
2016
Overview
Key Points
Cancer cells show increased consumption of and dependence on glutamine.
Glutamine metabolism fuels the tricarboxylic acid (TCA) cycle, nucleotide and fatty acid biosynthesis, and redox balance in cancer cells.
Glutamine activates mTOR signalling, suppresses endoplasmic reticulum stress and promotes protein synthesis.
Cancer cells may metabolize glutamate to α-ketoglutarate through one of two different pathways (glutamate dehydrogenase or aminotransferases), with aminotransferases potentially supporting a more biosynthetic and pro-growth phenotype.
Activation of oncogenic pathways and loss of tumour suppressors reprogramme glutamine metabolism in a tissue-dependent manner.
Targeting glutamine metabolism shows promise as an anticancer therapy. Compensatory glutamine metabolism induced by cancer therapies suggests that targeting glutamine metabolism may be used in combination therapy.
This Review provides an overview of glutamine metabolism and its involvement in tumorigenesis
in vitro
and
in vivo
, exploring the recent potential applications of basic science discoveries in the clinical setting.
The resurgence of research into cancer metabolism has recently broadened interests beyond glucose and the Warburg effect to other nutrients, including glutamine. Because oncogenic alterations of metabolism render cancer cells addicted to nutrients, pathways involved in glycolysis or glutaminolysis could be exploited for therapeutic purposes. In this Review, we provide an updated overview of glutamine metabolism and its involvement in tumorigenesis
in vitro
and
in vivo
, and explore the recent potential applications of basic science discoveries in the clinical setting.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
